#Lipotoxicity

[blueoaknx]

The Impact of High Fructose Corn Syrup on Mitochondrial Function

The Impact of High Fructose Corn Syrup on Mitochondrial Function:

Analysis

High fructose corn syrup (HFCS), a widely used sweetener derived from corn, has become a major component of the modern diet, especially in processed foods and sugary beverages. HFCS is composed of glucose and fructose in varying proportions, with HFCS-55 (55% fructose, 45% glucose) and HFCS-42 (42% fructose, 58% glucose) being the most common formulations. While the impact of HFCS on metabolic health has been widely discussed, recent studies have shown that it can also exert a detrimental effect on mitochondrial function. This technical analysis explores the biochemical mechanisms by which HFCS damages mitochondria, contributing to cellular dysfunction and a range of metabolic diseases.

Mitochondrial Physiology and Biochemical Function

Mitochondria are highly specialized organelles responsible for producing adenosine triphosphate (ATP), the primary energy currency of the cell, through oxidative phosphorylation (OXPHOS). This process occurs in the inner mitochondrial membrane and involves the electron transport chain (ETC) and ATP synthase. The mitochondria are also involved in regulating cellular metabolism, maintaining redox balance, calcium homeostasis, and apoptosis (programmed cell death). Mitochondrial dysfunction, characterized by impaired ATP production, altered mitochondrial dynamics (fusion/fission), and excessive reactive oxygen species (ROS) production, is a key factor in the pathogenesis of many chronic diseases, including obesity, insulin resistance, cardiovascular diseases, and neurodegenerative disorders.

Fructose Metabolism and Its Divergence from Glucose

The metabolism of fructose, particularly in the liver, diverges significantly from that of glucose, and it is this divergence that underpins much of the mitochondrial dysfunction associated with HFCS consumption. Unlike glucose, which is predominantly metabolized via glycolysis and the citric acid cycle (TCA cycle), fructose bypasses the rate-limiting step of glycolysis, catalyzed by phosphofructokinase-1 (PFK-1), and is instead phosphorylated by fructokinase to form fructose-1-phosphate. This rapid metabolism of fructose in the liver can overwhelm metabolic pathways and lead to the accumulation of intermediate metabolites such as dihydroxyacetone phosphate (DHAP) and glyceraldehyde, which can be further converted to fatty acids and triglycerides through de novo lipogenesis (DNL).

Excessive fructose consumption leads to the accumulation of triglycerides, particularly within hepatocytes, which is a hallmark of non-alcoholic fatty liver disease (NAFLD). The lipid accumulation in the liver, in turn, exacerbates mitochondrial dysfunction and oxidative stress, contributing to insulin resistance and a cascade of metabolic disorders.

Mechanisms of Mitochondrial Damage Induced by HFCS

Increased ROS Production

One of the most significant consequences of excess fructose metabolism is the elevated production of reactive oxygen species (ROS). ROS are byproducts of cellular respiration, primarily generated at complexes I and III of the electron transport chain. Under normal conditions, mitochondria have a robust antioxidant defense system, including enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, which help neutralize ROS. However, when cells are exposed to an overload of fructose, the liver mitochondria become overwhelmed, leading to excessive ROS generation.

Fructose metabolism increases the NADPH/NADP+ ratio, enhancing the activity of nicotinamide adenine dinucleotide phosphate (NADPH)-dependent oxidases such as NADPH oxidase (NOX), which further amplifies ROS production. These ROS cause oxidative damage to mitochondrial DNA (mtDNA), lipids in the mitochondrial membranes, and mitochondrial proteins. Such damage impairs mitochondrial function by decreasing mitochondrial membrane potential, disrupting the electron transport chain, and promoting mitochondrial fragmentation. Furthermore, mtDNA is particularly vulnerable to ROS due to its proximity to the electron transport chain and the lack of histone protection, leading to mutations that impair mitochondrial replication and protein synthesis.

Disruption of Mitochondrial Biogenesis

Mitochondrial biogenesis refers to the process by which new mitochondria are synthesized within a cell to meet the energy demands. This process is tightly regulated by several transcription factors, most notably peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α). PGC-1α activates the transcription of nuclear and mitochondrial genes involved in energy metabolism, mitochondrial dynamics, and antioxidant defenses.

Fructose consumption has been shown to inhibit PGC-1α expression in both liver and skeletal muscle cells. Reduced PGC-1α levels lead to impaired mitochondrial biogenesis, which limits the ability of cells to adapt to increased energy demands. This is particularly concerning in tissues with high metabolic demands, such as muscle, heart, and liver, where impaired mitochondrial function can exacerbate energy deficits and lead to insulin resistance, fatty liver disease, and other metabolic disorders.

Mitochondrial Permeability Transition and Apoptosis

Chronic exposure to high levels of fructose can lead to mitochondrial permeability transition (MPT), a process in which the mitochondrial inner membrane becomes permeable to ions and small molecules, disrupting mitochondrial function. MPT is typically induced by excessive ROS production, calcium overload, or changes in the mitochondrial membrane potential. The opening of the mitochondrial permeability transition pore (MPTP) leads to the loss of mitochondrial membrane potential, uncoupling of oxidative phosphorylation, and the release of pro-apoptotic factors such as cytochrome c into the cytoplasm. This, in turn, activates the caspase cascade, promoting apoptosis.

In the context of HFCS-induced mitochondrial dysfunction, increased ROS and altered metabolic intermediates, such as ceramides, may trigger MPT and apoptotic pathways, leading to cell death and tissue damage. In tissues such as the liver and pancreas, this can exacerbate the pathological progression of fatty liver disease and insulin resistance.

Fatty Acid Accumulation and Impaired Beta-Oxidation

Excessive fructose consumption induces de novo lipogenesis (DNL) in the liver, leading to an increase in the synthesis of fatty acids, which are esterified into triglycerides and stored within hepatocytes. This accumulation of lipids can overwhelm the capacity of mitochondria to oxidize these fatty acids via beta-oxidation, leading to mitochondrial dysfunction. The accumulation of lipotoxic intermediates such as ceramides and diacylglycerols further impairs mitochondrial function by inhibiting key enzymes involved in mitochondrial energy production.

Moreover, the excess fatty acids can impair mitochondrial membrane fluidity, reducing the efficiency of oxidative phosphorylation. The lipid-induced mitochondrial dysfunction leads to further oxidative stress, creating a feedback loop that exacerbates the metabolic disturbances caused by high fructose intake.

Clinical Implications of HFCS-Induced Mitochondrial Dysfunction

The long-term consumption of HFCS has profound implications for human health, particularly in the context of metabolic diseases:

Insulin Resistance and Type 2 Diabetes: HFCS-induced mitochondrial dysfunction, particularly in liver and muscle cells, contributes to impaired insulin signaling and glucose homeostasis. As mitochondrial function declines, cells become less responsive to insulin, leading to insulin resistance, a precursor to type 2 diabetes.

Non-Alcoholic Fatty Liver Disease (NAFLD): The accumulation of fat in the liver, driven by increased fructose metabolism, leads to mitochondrial damage and dysfunction, which exacerbates the progression of NAFLD to non-alcoholic steatohepatitis (NASH), a more severe form of liver disease.

Cardiovascular Disease: Mitochondrial dysfunction in cardiomyocytes can impair ATP production, leading to reduced contractile function and the progression of cardiovascular disease. The increased oxidative stress and inflammatory mediators associated with mitochondrial damage also contribute to vascular injury and atherosclerosis.

Neurodegenerative Diseases: Impaired mitochondrial function in neurons, driven by high fructose intake, may contribute to neurodegenerative diseases such as Alzheimer's and Parkinson's disease, as mitochondria play a critical role in maintaining neuronal health.

Conclusion

High fructose corn syrup exerts a significant impact on mitochondrial function through several interconnected mechanisms. These include the increased production of reactive oxygen species (ROS), inhibition of mitochondrial biogenesis, induction of mitochondrial permeability transition, and the accumulation of toxic lipid intermediates. These disruptions in mitochondrial homeostasis contribute to the development of insulin resistance, non-alcoholic fatty liver disease, and other chronic metabolic diseases. Addressing the widespread consumption of HFCS and reducing dietary fructose intake could be crucial in mitigating mitochondrial dysfunction and preventing associated metabolic disease

[neverquiteedenstudyblr]

Had a really interesting lecture about this and how obesity isn't really a choice given our current food landscape and how we are wired biologically, or at least not the type of choice people tend to imagine. It's way harder for some people to rid themselves of fat than others, even if it's at the level of it affecting their health and current quality of life. I've asked for a supervision with the lecturer to better understand this topic.

There's also different levels of fat that is able to be stored by every body, and once you reach that capacity that's when you start experiencing symptoms of metabolic syndrome. For example, lipodystrophy prevents people from storing and maintaining healthy subcutaneous fat (often only in certain areas) resulting in their stores being maximised and overloaded more quickly despite not necessarily having large amounts of fat on their bodies. This results in lipotoxicity (fats being stored in areas other than fat tissue, resulting in tissue damage ie fatty liver disease) and insulin insensitivity.

We also talk about metabolically healthy and unhealthy obesity, where the first is associated with hyperplasia of the fat tissue, and the second involves hypertrophy of fat cells and inflammation.

You know I wish fatphobia was less pervasive. Even among people who consider themself as progressive, it's rampant. So quick reminder. No it's actually not easy to stop being fat, and it sucks that we are treated differently for something we really can't control. Shaming a fat person for being fat, and shaming them for not having the "willpower" to become skinny- is bigotry. And if all you talk to fat people about is weight loss and dieting- congratulations! You're being a dick! Stop.

[yeast-papers]

Formation of giant ER sheets by pentadecanoic acid causes lipotoxicity in fission yeast

BioRxiv: http://dlvr.it/TC34Gw

[biomedres]

Differential Effects of Unsaturated Fatty Acids and Saturated Fatty Acids on Lipotoxicity and Neutral Lipid Accumulation in Neuro-2a Cells

Differential Effects of Unsaturated Fatty Acids and Saturated Fatty Acids on Lipotoxicity and Neutral Lipid Accumulation in Neuro-2a Cells in Biomedical Journal of Scientific & Technical Research

https://biomedres.us/fulltexts/BJSTR.MS.ID.006017.php

Long-chain free fatty acids (FFA) play many important roles in cell growth and metabolism. Accumulation of excess saturated fatty acids (SFA) leads to deleterious lipotoxic effects in non-adipose tissues while unsaturated fatty acids (UFA) often exert protective effects against SFA lipotoxicity, yet the lipotoxic effects of SFA in neuronal cells have not been well characterized. This study examined the differential effects of SFA and UFA on the viability of Neuro-2a (N2a) cells and the accumulation of neutral lipids in these cells. Our study found that all the UFA tested, namely oleic acid (OA), linoleic acid (LA), α-linolenic acid (ALA), and docosahexaenoic acid (DHA), were able to abolish PAinduced decrease in cell viability regardless of the position of the double bond or degree of unsaturation, and that 200 μM LA, OA, and DHA significantly enhanced the amount of neutral lipid staining than BSA control while PA did not, suggesting that LA, OA, and DHA, but not PA, increased the amount of neutral lipid synthesis and accumulation. The neutral lipid staining also appeared more in particulates in UFA-treated cells than PAtreated cells, suggesting that UFA, but not PA, enhanced LD formation. We also found that the amount of neutral lipid staining in cells co-treated with UFA and PA was comparable to that in cells treated with BSA or PA alone, and that the neutral lipid staining in cells co-treated with UFA and PA appeared more concentrated in particulates than PA-treated cells, suggesting that UFA may not enhance neutral lipid accumulation, but may increase LD formation in PA-treated cells. Our results suggest that UFA and SFA have differential effects on cell viability, neutral lipid accumulation, and LD formation in N2a cells. Further studies will be needed to examine the role of LD formation in UFA protection against PA lipotoxicity.

For more articles in Journals on Biomedical Sciences click here bjstr

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[healthwellwisher]

 Reignite Review - Burn Fat Naturally

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►➤► Benefits –Weightloss Supplement

►➤►Aftereffects — NA

►➤►Accessibility —Online

►➤►Rating — 5/5

►➤►Official Website (Sale Is Live) ⤖ Click Here to Order Now

ReIgnite tablets include all-natural and powerful fat-burning chemicals. ReIgnite's primary objective is to promote mitochondrial development. These pills may enhance energy and minimise ageing and body fat in a short period of time.

According to a survey conducted in 2020, approximately 30 percent of adults in the United States are obese. These figures demonstrate that the majority of individuals are obese or are becoming obese.

If you suffer from a cellular energy crisis and metabolic sluggishness, we may have the ideal solution for you. Yes, you can reduce your unexplained weight and eradicate stubborn belly fat through movement.

ReIgnite tablets include all-natural and powerful fat-burning chemicals. ReIgnite's primary objective is to promote mitochondrial development. These pills may enhance energy and minimise ageing and body fat in a short period of time.

How can ReIgnite improve the health of mitochondria?

Due to their involvement in cellular energy production, mitochondria are known as the "powerhouses of the cell." They produce the majority of the cell's adenosine triphosphate (ATP), which is essential for a variety of metabolic activities. Mitochondria serve a crucial function in our cells, thus it should come as no surprise that mitochondrial health is crucial to our overall health and wellbeing.

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Mitochondrial dysfunction can be caused by many circumstances, including obesity, poor food, pollutants, stress, and age. However, obesity is one of the most potent. The buildup of fat in mitochondria is one of the processes by which obesity contributes to mitochondrial dysfunction. This process, known as lipotoxicity, affects the mitochondria's ability to generate energy, resulting in cell death and tissue damage. Inflammation associated with obesity may potentially lead to mitochondrial dysfunction.

By accumulating reactive oxygen species, obesity can also cause mitochondrial dysfunction (ROS). ROS are metabolic byproducts that can cause damage to a cell's DNA, proteins, and lipids. Excessive quantities can overwhelm the body's ability to heal damage, resulting in mitochondrial malfunction and cell death.

These pathways collectively explain how obesity can result in mitochondrial dysfunction. Additionally, the chance of developing diabetes and cardiovascular disease is raised.

ReIgnite is a potent antioxidant that protects cells from damage caused by reactive oxygen species (ROS) and obesity. Boosting ATP production and mitochondrial health is an additional advantage. It can aid in the prevention of age-related illnesses and enhance general health.

Following are some of ReIgnite's essential characteristics that assist users lose body fat and gain confidence in the brand.

100% Organic Blend

ReIgnite's inclusion of 100% natural plant extracts is one of its most advantageous qualities. Such natural extracts assist the body in adhering to a healthy path for fat loss and mitochondrial biogenesis.

This nutritional supplement reduces obesity with ginger extract. According to the company, ReIgnite can aid in fat burning, hunger suppression, and metabolism enhancement. In addition, ginger extract is a natural substance that has been used for millennia in Traditional Chinese Medicine.

This pill contains large volumes of ginger extract to accelerate the process.

For optimal benefits with ReIgnite, you should take the supplement for at least ninety days. Therefore, the professionals have made it simpler for you to order in three different quantities. Moreover, ordering in bulk results in substantial discounts.

As a result, it is a win-win situation because you may order in bulk and pay less per bottle. A single bottle is sufficient for thirty days and costs $69 per unit.

However, if you choose for a 90-day supply and purchase three bottles, you will only spend $59 a bottle. In addition, the organisation offers an additional discount if you order a supply for eighty days at once. If you purchase six bottles at once, you will only be charged $49 per bottle.

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Authenticated and Safe Transactions

The professionals at ReIgnite are aware of the concerns of internet shoppers. The majority of consumers are concerned about identity theft and fraud while submitting financial information online.

However, these concerns are unnecessary when purchasing ReIgnite. The official website of the organisation employs a reliable security system to safeguard your information. In addition, you can make payments with Visa, Master Card, PayPal, or American Express.

60-Day Money-Back Assurance

ReIgnite also offers a money-back guarantee for up to sixty days, which is an admirable feature. Not all makers of nutritional supplements offer such luxuries. Nonetheless, any professional manufacturer who is confident in the quality of their product will give a trial period.

You can utilise these sixty days to determine whether ReIgnite is beneficial for your body type. You can give a good review if you notice positive changes in your physique. You may request a refund within sixty days of your purchase if you observe any negative effect or no effect at all.

How Does Boosting Mitochondrial Function Reduce Obesity and Weight Gain?

In wealthy nations throughout the world, obesity and weight increase are important issues. This not only negatively impacts people's health, but also increases health risks and treatment costs.

Mitochondrial boosting is one potential solution to this problem. By increasing mitochondrial efficiency, it may be feasible to minimise the amount of fat stored in the body. In addition, mitochondrial improvement may contribute to an increase in the quantity of energy burned by the body.

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As a result, this strategy may be an effective method for combating obesity and weight gain. In addition, mitochondrial improvement may potentially reduce the risk of chronic diseases such as colorectal cancer, cardiovascular disease, and diabetes.

Conclusion

With the ever-increasing prevalence of obesity, diabetes and other heart-related issues are on the rise. Obesity inhibits mitochondrial enhancement in the body, which is one of its key downsides.

However, if we use supplements for mitochondrial biogenesis, such as ReIgnite, we can reverse obesity and recover our ideal body shape. You can try ReIgnite for at least ninety days with ordinary water in the morning and observe the results for yourself.

Affiliate Disclosure: The links in this product review may result in a small fee if you decide to purchase the suggested product at no additional cost to you. This will be used to assist our research and editorial teams. Please note that we only propose premium products.

[obesitycoach]

According to William Davis, the author of Wheat Belly: “Carbohydrates trigger insulin release from the pancreas, causing growth of visceral fat; visceral fat causes insulin resistance and inflammation. High blood sugars, triglycerides, and fatty acids damage the pancreas. After years of overwork, the pancreas succumbs to the thrashing it has taken from glucotoxicity, lipotoxicity, and inflammation, essentially “burning out,” leaving a deficiency of insulin and an increase in blood glucose—diabetes.”

[cytoscape-publications]

Magnesium Isoglycyrrhizinate Reduces Hepatic Lipotoxicity through Regulating Metabolic Abnormalities. Lu, et al., International journal of molecular sciences doi: 10.3390/ijms22115884.

[tummylite]

Why worry about your Waistline ?

Excess fat around your belly is especially dangerous for your health.

Doctors have warned that a big belly is more harmful to your health than extra fat in your hips and thighs.

A growing number of Americans are now oversized belly according to the latest statistics from the CDC.

The average waist circumference for men is now 40.2 inches, up from the 39 inches recorded in the last survey, which was done in 1999–2000.

Women's waist measurements also rose — from an average of 36.3 to 38.6 inches.

That means that a majority of Americans now have belly sizes that put them at high risk

"As your waistline expands, so does your risk of cardiovascular disease,"

explains Dr. Osama Hamdy, medical director of the Obesity Clinical Program at Harvard-affiliated Joslin Diabetes Center.

Belly fat — what doctors refer to as visceral fat — turns out to be very different from fat that accumulates in the hips and thighs, he explains.

How to measure your waistline.

To measure your waist accurately, exhale and wrap a measuring tape around your bare abdomen just above the upper border of your hipbone, which you can easily feel on both sides.

Waist-to-Hip Ratio ( WHR )

Measure your hips by putting the tape measure around the widest part of your buttocks.

Then, divide your waist size by your hip size.

Measurements that signal high risk

For Women

Waist (inches) : 35 or more

Waist-to-hip ratio : 0.9 or more

For Men

Waist ( inches ): 40 or more

Waist-to-hip ratio : 1.0 or more

Location matters

Belly fat accumulates deep within the abdominal cavity, filling the space between the organs.

When these fat cells break down, they shower the portal vein (the vein that carries blood from the intestinal area to the liver) with free fatty acids and other substances.

The resulting state of "lipotoxicity" affects the nearby pancreas, hampering its ability to produce insulin, the hormone that carries glucose into the body's cells.

Lipotoxicity also promotes insulin resistance, in which the body's muscle and liver cells don't respond adequately to normal levels of insulin. As a result, blood sugar levels rise, boosting the risk for type 2 diabetes.

In addition, when these misplaced fat cells die, cells that serve as the cleanup crew release inflammatory substances called cytokines.

"Those cytokines are one reason people develop atherosclerosis, the underlying cause of cardiovascular disease," says Dr. Hamdy.

In contrast, fat that collects in the hips and thighs seems to be less harmful and less prone to diabetes and heart disease than people with bigger bellies.

Who is vulnerable?

Your genes, ethnic background, and sex all influence how likely you are to accumulate visceral fat.

Girth control

While there's no magic formula for losing belly fat, a reduced-carbohydrate diet can be helpful, particularly if you have type 2 diabetes, says Dr. Hamdy.

You don't need to avoid all carbs — just stay away from those that quickly spike your blood sugar levels and encourage your body to store fat. These three sources are the major culprits:

Sugar.

Anything made with added sugar — cookies, cakes, pastries, ice cream, soft drinks, canned juices, and the like.

White flour.

The most commonly consumed examples (and worst offenders) are what Dr. Hamdy refers to as the "P's and B's": pasta, pizza, bread, and bagels.

Starchy foods. 

White potatoes, rice, and corn.

The basic idea is to limit your food intake to a shorter-than-normal time frame.

Dr. Hamdy suggests.

And don't forget to do regular exercise (both aerobic and muscle-strengthening), which can help you burn extra calories and helps preserve lean muscle mass.

Visit www.tummylite.com and show your meal pictures and we will advise you how to eat to reduce waistline.

It is Free.

[kramlabs]

On a long enough timeline, eating vegetable oils will give you Covid-19 like symptoms. And when you do get Covid, you will suffer.

-vegetable oils “depolarize mitochondria, inhibit complexes I and V, decrease ATP, release intracellular calcium, and increase in- flammatory mediators... made us explore lipotoxicity during severe COVID-19. “

“Mice administered linoleic acid (vegetable oil) but not the saturated fatty acid C16:0 (saturated animal fat, stearic) developed hypoalbuminemia (lower oxygen saturation...”

“Mice given omega 6 vegetable oils (c18’s), but not saturated animal fat (stearic C16:0), developed leucopenia, lymphopenia, lymphocytic injury, relative thrombocytopenia, hypercytokinemia, elevated alanine aminotransferase levels, hypoalbuminemia, hy- pocalcemia, shock, and renal failure resembling lethal COVID-19”

“Mortality From Coronavirus Disease 2019 Correlates With Dietary Unsaturated Fat (vegetable oil) Intake; Saturated Fat (animal) Is Protective”

https://www.gastrojournal.org/article/S0016-5085(20)34727-2/fulltext

PDF

[crimsonpublishersobesityjourna]

The Role of Obesity-Induced Inflammation in Pancreatic β-Cell Dysfunction and Death-Crimson Publishers

The Role of Obesity-Induced Inflammation in Pancreatic β-Cell Dysfunction and Death by Danielle Melloul in Intervention in Obesity & Diabetes

Type 2 diabetes (T2DM) is frequently associated with elevated levels of lipids, in particular plasma free fatty acids and toxic lipid metabolites in muscle, liver, adipocytes, pancreatic islets and arterial tissues, contributing to insulin resistance and pancreatic islet β-cell dysfunction. The pathophysiology of T2DM is increasingly being linked with inflammatory mediators such as cytokines and chemokines as well as with changes in the number and activation state of macrophages/monocytes leading to β-cell dysfunction and subsequently to insulin insufficiency. The prevalent product of the cyclooxygenase 2 (COX-2) enzyme PGE2, controls numerous physiological functions through a family of cognate G proteincoupled receptors (EP1-EP4). The EP3 receptor which is selectively upregulated in islets of T2DM individuals, is upregulated under lipotoxic conditions and is involved in β-cell dysfunction and demise. This EP3 target presents a new approach to delay the progression of T2DM disease by preserving the pancreatic β-cells.

For more about in Crimson Publishers, please click on the link: https://crimsonpublishers.com/peer-review-process.php

For more articles in Journal of  Diabetes and Obesity, please click on below link: https://crimsonpublishers.com/iod/

Follow On Linkedin : https://linkedin.com/in/chyler-henley-ba9623175

Follow On Medium : https://medium.com/crimson-publishers/crimson-publishers-journals-f29e22da8f5c

Please click on high impact journals in Crimson Publishers

[bettybxiong]

Can nicotinamides address liver cell death and treat non-alcoholic fatty liver disease?

(Natural News) Nicotinamide, also known as niacinamide, is a form of vitamin B3 found in food and used as a dietary supplement. A study published in the journal Nutrition Research suggested that this nutrient can help prevent liver cell death and treat non-alcoholic fatty liver disease (NAFLD). According to the study, nicotinamide exhibits anti-lipotoxic activity. Lipotoxicity, which...

from NaturalNews.com https://ift.tt/2M9Qnyr from Betty Xiong https://ift.tt/2Oauyl3

[zeonlifesciences]

The Potential Benefits of Grape Seed Extract for Immune Support

Everyone loves grapes. But are you aware that one of the healthiest parts of a grape, the seed is often discarded?

Grape Seed Extract

Grape seeds and their extract have been the focus of many research studies which evaluates their many health benefits. These benefits range from supporting healthy blood pressure levels, providing antioxidant protection to, supporting overall heart health. Grape seed extract have become popular dietary supplements in recent years because they are pharmacologically active components which have antioxidant properties. This provides protection to cells from free radicals. Grapes plant contains the powerful antioxidant Oligomeric proanthocyanidins (OPCs), which benefits many health conditions. Grape Seed Extract supplements contain the perfect blend of tannins and Oligomeric proanthocyanidin complexes, which provides exceptional benefits for our nutritional health.

Benefits of Grape seed extract-

Strengthens immune system- Helps the body to produce a potent antioxidant that protects DNA and strengthens the immune system. Also, helps humans to boost their immunity.

Reduces High blood pressure – This is associated with the decrease in systolic and diastolic pressure. This reduces bad cholesterol as well. This was found to be a safe and effective nutraceutical ingredient to support healthy blood pressure levels.

Diabetes management- Helps to protect pancreatic cells from lipotoxic effect to reduce normal insulin secretion.

Protects inflammation- Helps to reduce inflammation also.

Skin care- Helps fight cell damage caused by harmful free radicals. This helps skin to get protection from UV rays. As a potent antioxidant, this supplement is believed to provide the best nutrition for the skin.

Heart- High dose of GSE cause an increase in blood circulation, which helps improving cardiovascular health. Also this improves blood oxygen circulation throughout the body.

Weight management- Other than antioxidant properties, it also helps to reduce fat deposits and reduce the absorption of fat from our diets.

Boosts brain power- This also helps to improve concentration, memory and mood.

Nutrients in Grape seed Extract-

Grape seed extract is rich in various numerous minerals, but its most potent nutrients are antioxidants like OPCs. Other than these following are the nutrients in grape seed extract-

Vitamin E

Linolenic acid

Potassium

Copper

Phosphorus

Calcium

Zinc

Magnesium

Iron

In their natural form, Grape seeds have approximately-

35% Fiber

3% minerals

11% Protein

7% Water

20% Oils

There is no dose mentioned for grape seed extract, but it could be take 100 to 300 mg per day.

Conclusion-

In conclusion this blog shows that grape seed extract helps in so many ways, specially shows antioxidant effect which helps to boost immunity to fight against so many diseases. The GSE is safe, natural and cost effective treatment.

If you looking for any third party manufacturer who can give you best possible formulations containing Grape seed extract. Then Zeon Lifesciences is the answer for all your questions.

Zeon use grape seed extract in so many formulation such as Immunity booster, bone health, Multivitamins, joint care, skin health etc.

Contact Zeon Lifesciences to get the best quality products.

[tuncaydelibasi]

The sensitivity of insulin changes during the replacement of leptin

Leptin can also increase the sensitivity of insulin, not just through reducing lipotoxicity and adiposity as well as insulin-independent actions both peripherally and centrally. Leptin can also reduce the manufacturing of glucose which contributes to its effect of lowering the level of glucose.

In addition to engaging in exercises, getting rid of body fat will increase the sensitivity of insulin. Look for foods with more fiber and lower GI and the glycemic load, which can help increase the sensitivity to insulin. Other strategies to improve insulin sensitivity is to sleep enough, and to decrease stress levels.

What triggers increased insulin sensitivity?

Chromium, Berberine magnesium and berberine supplements can increase insulin sensitivity. Resveratrol may increase the sensitivity of insulin, especially in those with type 2 diabetes.

As insulin levels rise and the body is unable to keep on burning fats for fuel, and also encourages the storage of food items in the form of fat. This is why, so long as the diet is rich in carbohydrates and fats, the body doesn't have the chance to burn off its own fats, which makes the process of losing weight more difficult.

Two kinds, or classes of diabetes medications increase the number of cells or more sensitive to insulin. These are the biguanides and the thiazolidinediones (TZDs).

How does leptin affect insulin levels?

In addition, leptin hinders insulin secretion via PI3K-dependent stimulation of the phosphodiesterase 3B (PDE3B) and also by reduced cAMP levels, thereby hindering the protein kinase A (PKA) pathway that responsible for controlling Ca2+ channels as well as exocytosis (Marroqui and co. 2012).

Insulin is a key anabolic hormone, and it is known to promote muscle growth. The treatment of insulin in people with uncontrolled diabetes can increase muscle mass, whereas the deficiency of insulin causes the loss of muscle mass.

Source: American Journal of Physiology-Endocrinology and Metabolism

[rnomics]

Nutrients, Vol. 14, Pages 3871: CCN1/Integrin α5β1 Instigates Free Fatty Acid-Induced Hepatocyte Lipid Accumulation and Pyroptosis through NLRP3 Inflammasome Activation

Hyperlipidemia with high blood levels of free fatty acids (FFA) is the leading cause of non-alcoholic steatohepatitis. CCN1 is a secreted matricellular protein that drives various cellular functions, including proliferation, migration, and differentiation. However, its role in mediating FFA-induced pro-inflammatory cell death and its underlying molecular mechanisms have not been characterized. In this study, we demonstrated that CCN1 was upregulated in the livers of obese mice. The increase in FFA-induced CCN1 was evaluated in vitro by treating hepatocytes with a combination of oleic acid and palmitic acid (2:1). Gene silencing using specific small interfering #RNAs (#siRNA) revealed that CCN1 participated in FFA-induced intracellular lipid accumulation, caspase-1 activation, and hepatocyte pyroptosis. Next, we identified integrin &alpha;5&beta;1 as a potential receptor of CCN1. Co-immunoprecipitation demonstrated that the binding between CCN1 and integrin &alpha;5&beta;1 increased in hepatocytes upon FFA stimulation in the livers of obese mice. Similarly, the protein levels of integrin &alpha;5 and &beta;1 were increased in vitro and in vivo. Experiments with specific #siRNAs confirmed that integrin &alpha;5&beta;1 played a part in FFA-induced intracellular lipid accumulation, NLRP3 inflammasome activation, and pyroptosis in hepatocytes. In conclusion, these results provide novel evidence that the CCN1/integrin &alpha;5&beta;1 is a novel mediator that drives hepatic lipotoxicity via NLRP3-dependent pyroptosis. https://www.mdpi.com/2072-6643/14/18/3871?utm_source=dlvr.it&utm_medium=tumblr

[jasondouglasnewyork-blog]

keto BHB 800 Weight Loss : Burn Fat Faster - Shark Tank Diet

The advertiser zone of the adiponectin quality seems to have an utilitarian responsive part for PPARγ (36, 37). The irregularity of adiponectin could be a delayed consequence of changes in plan of PPARγ mRNA by transactivation of PPARγ by linoleic hurting. Future examinations concerning adipokine period with dietary-oil supplementation might be a key determinant in right hand dietary fat quality with decreasing weight and harming metabolic gets.

Postmenopausal ladies are at generously broadened danger of making insulin opposition (4). Dietary sprinkled fat has been related with reduced edges insulin affectability (38). Regardless, Keto BHB 800 is diminishing how polyunsaturated fats add to Keto BHB 800 Shark Tank redesigned insulin affectability. Our investigation has shown that SAF hack down glycemia and diminished HOMA-IR, which might be credited to bring down trunk fat mass, made adiponectin, or both.

In moving of the customary impact of trunk fat mass with glycemic control, instinctual fat related over a 7-y period was related with key incapacitating of glucose-insulin homeostasis after redesign for complete fat change (39). The impact of making ordinary load with a decreasing of glycemic control may make lipid supply to the liver and β cells, all around called a lipotoxic influence (40). Lipotoxicity can induce created hepatic glucose creation and β cell disappointment,

The two of which lead to poor glycemic control.

Prior investigations with Keto BHB 800 in Zucker diabetic smooth rodents have appeared Keto BHB 800 could change the difference in disabled glucose Keto BHB 800 versatility and hyperinsulinemia. Thinking about all things, brace considers have demonstrated that t10c12- Keto BHB 800 could generally incite hypnotized insulin affectability in human subjects when fat hacking down impacts were seen.

Taking after examinations have displayed blended outcomes: One other investigation demonstrated Keto BHB 800 stores up glucose versatility , while another demonstrated no such impact.

In our associate, we didn't watch an impact of Keto BHB 800 on surrogate markers of insulin affectability (Table 4). In addition, not change nonesterified free unsaturated fats or triglyceride focuses (information not appeared). Notwithstanding the way that weight diminishment >7% is appeared to overhaul relationship of glycemia in individuals with T2DM (45), Keto BHB 800 makes the inclination that the load and fat dissatisfaction by Keto BHB 800 in our examination was not of Keto BHB 800 ssy degree to upgrade markers of glycemia. Read more …

There were a couple constrainments to our focus system. In any case, our examination individuals was amazing postmenopausal ladies, annihilating likelihood to add to up our outcomes to nonobese people or to premenopausal nondiabetic ladies. In like way, Keto BHB 800 Reviews we considered centrality and supplement orders with the usage of accentuated 3-d diet records that may not thoroughly reflect clear changes in calories that may have occurred in light of the consistently progress of 72 kcal from oil. Another check is the decision of 16-wk cream mediations that may not give mind blowing time to demonstrate most astounding outcomes on changes in results estimated. At long last, we see that there are blocks that occur in a free-living masses that could be better estimated in a controlled condition.

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Is Teal farms keto Another Scam?

This investigation is the first to show that such an unnoticeable total (≈1-2/3 teaspoon or 8 mL) of a linoleic acid– rich oil may mean impact body s  Teal Farms Keto  in ladies. Notwithstanding the manner in which that  Teal Farms Keto diminished complete body adiposity, SAF diminished  Teal Farms Keto nk fat mass in both eating routine periods. The hardship found Teal Farms Keto Reviews in our investigation (1.20 and 1.90 kg) proposes a standard loss of 6.3% of beginning fat mass of the cutoff compartment zone. To the degree anyone is concerned; this centrality of diminishing has not been tended to in an intervention that utilized a linoleic acid– rich oil. In addition, SAF broadened absolute body incline tissue mass (choices averaging 1.4 and 0.6 kg, a ≈1.6% advance from beginning examination mass).

Unmitigated, the impact of SAF was free of eating routine or advancement changes (Table 5). Beginning late, an eating routine containing corn oil displayed a Teal Farms Keto twofold impact on adipogenesis in mice: In a high-starch diet, corn oil updated adipogenesis, yet in a high-protein diet corn oil was antiadipogenic in mice (17). Regardless of the course that there was no detainment in dietary sugar or protein use between eating routine packs in either check calories period, the joint effort among SAF and explicit macronutrients was not attempted in our examination.

Starting currently examined, postmenopausal ladies are at opened up threat of making focal essentialness (3, 4). Anthropometric estimations, including guts edge and SAD, did not demonstrate a key diminishment in stomach fat in our investigation. Regardless, with the usage of DXA, we found reduced  Teal Farms Keto nk fat amidst SAF supplementation. Neighborhood contrasts if there should be an occasion of worth have been related with changes of adipokine period (33). Adiponectin might be related with subcutaneous fat stations. In the present investigation, SAF on an amazingly basic dimension expanded adiponectin fixations by a normal of 20.3%, anyway no crucial changes in adipokines were seen with, Read more …

 Teal Farms Keto supplementation. Regardless of the way that a development in adiponectin focuses was watched, we were not set up to see changes of subcutaneous fat (eg, fat mass of hips, thighs, etc), as estimated by DXA. One illuminating is that the difference in serum adiponectin by SAF is a concise unavoidable aftereffect of a balanced dimension of normal fat: subcutaneous fat (34); in any case, DXA development can't see trademark and subcutaneous fat terminals. Additionally, linoleic ruinous is an unassuming ligand for peroxisome proliferator-prompted receptor γ (PPARγ) (35). Portrayal of adiponectin is had with the PPARγ ligands (eg, thiazolidinediones).

The advertiser zone of the adiponectin quality seems to have an utilitarian responsive part for PPARγ (36, 37). The irregularity of adiponectin could be a delayed consequence of changes in plan of PPARγ mRNA by transactivation of PPARγ by linoleic hurting. Future examinations concerning adipokine period with dietary-oil supplementation might be a key determinant in right hand dietary fat quality with decreasing weight and harming metabolic gets.

Postmenopausal ladies are at generously broadened peril of making insulin opposition (4). Dietary sprinkled fat has been related with lessened edges insulin affectability (38). Regardless, it is diminishing how polyunsaturated fats add to redesigned insulin affectability. Our examination has shown that SAF hack down glycemia and decreased HOMA-IR, which might be credited to bring down  Teal Farms Keto nk fat mass, made adiponectin, or both.

In moving of the customary impact of  Teal Farms Keto nk fat mass with glycemic control, instinctual fat related over a 7-y period was related with key weakening of glucose-insulin homeostasis after redesign for all out fat change (39). The impact of making ordinary load with a decreasing of glycemic control may make lipid supply to the liver and β cells, all around called a lipotoxic influence (40). Lipotoxicity can instigate created hepatic glucose creation and β cell disappointment,

The two of which lead to poor glycemic control.

Prior investigations with  Teal Farms Keto in Zucker diabetic smooth rodents have demonstrated that  Teal Farms Keto could change the difference in disabled glucose versatility and hyperinsulinemia (14, 41). Thinking about all things, brace considers have demonstrated that t10c12-  TEAL FARMS KETO  could generally incite hypnotized insulin affectability in human subjects when fat hacking down impacts were seen (42).

Taking after examinations have displayed blended outcomes: One other investigation demonstrated  Teal Farms Keto stores up glucose flexibility (43), while another demonstrated no such impact (44). In our assistant, we didn't watch an impact of  Teal Farms Keto on surrogate markers of insulin affectability (Table 4). Furthermore, not change nonesterified free unsaturated fats or triglyceride focuses (information not appeared). In spite of the way that weight diminishment >7% is appeared to update relationship of glycemia in individuals with T2DM (45), it makes the inclination that the load and fat dissatisfaction by  Teal Farms Keto in our examination was not of  Teal Farms Keto ssy degree to upgrade markers of glycemia.