#peroxisome

[gl1tt3r-gutz-and-r0b0tz-sl]

Here's some more old art lol! This was for a biology project earlier this year. It was about organelles. Some of it may not be 100% accurate but I got a 100! so that's all that counts :'>

IT WAS MY EXCUSE TO DRAW CUTE GIRLS IN CAMOUFLAGE AND MAKE DOOMED YURIs 😭😭😭😭😭😭😭

THIS WAS WHEN I FINISHED WATCHING LAND OF THE LUSTROUS.

[dark-in-the-rooms]

hurr hurr I'm a human body hurr hurr I'm gonna solve all my problems using mucus

[cytgen]

Abstract For the first time, the effect of 5- and 10-day soil flooding on the ultrastructure of the leaf mesophyll cells of the psammophyte desert madwort (Alyssum desertorum L.) was investigated. The seeds for the experiments were collected from plants of dry sandy areas of the gully slopes of the ravine forest in the steppe zone of the Dnipropetrovsk oblast. It is shown that a characteristic feature of the leaf photosynthetic cells of this species is the presence of single and large, up to 6 pm, peroxisomes, which are in close contact with chloroplasts and mitochondria, playing a key role in photorespiration. The general organization of palisade parenchyma cells on days 5 and 10 of soil flooding is similar to that in the control. A slight decrease in the size of peroxisomes on day 5 of flooding and its increase on day 10 and more often formation of multivesicular structures (assembly of endomembranes) in the vacuole, which is considered as an autophagy enhancement of the cytoplasm under hypoxia, were noted. Differences in the ultrastructure of chloroplasts under the influence of soil flooding consisted in a significant, almost twofold increase in transient starch, the size and number of plastoglobules, especially on day 10, and swelling of granal and stroma thylakoids on day 10. Changes in the ultrastructure of desert madwort chloroplasts under the influence of soil flooding coincide with those of mesophytes studied in this respect. The obtained data on the chloroplast ultrastructure of desert madwort psammophyte prove the functioning of the photosynthetic apparatus in conditions of short-term soil flooding, which contributes to the survival of seedlings. The subsequent yellowing of leaves and death of plants indicates, as is assumed, the lack of systemic adaptation, primarily metabolic, that is, the transition to anaerobic metabolism, in this species to long-term hypoxia.

[tenth-sentence]

Variants of superoxide dismutase are found in chloroplasts, peroxisomes, mitochondria, cytosol, and apoplast.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[whats-in-a-sentence]

In plants, JA is synthesized from linolenic acid (18:3), which is released from membrane lipids and then converted to JA, as outlined in Figure 23.18.

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[bpod-bpod]

Vital for Immunity

Importance of peroxisomes – organelles inside cells that are involved in lipid metabolism – for immune cell development and immune responses revealed by defects seen in a peroxisome-deficient mouse model of the congenital disorder Zellweger disease

Read the published research article here

Image from work by Brendon D. Parsons and Daniel Medina-Luna, and colleagues

University of Alberta, Department of Laboratory Medicine and Pathology, Edmonton, AB, Canada

Image originally published with a Creative Commons Attribution – NonCommercial – NoDerivs (CC BY-NC-ND 4.0)

Published in Cell Reports, February 2024

You can also follow BPoD on Instagram, Twitter and Facebook

[boyfhee]

if i do well on today's test, i will change my user

[hellsite-proteins]

WoLF PSORT is an extension of the PSORT II program for protein subcellular localization prediction, which is based on the PSORT principle. WoLF PSORT converts a protein's amino acid sequences into numerical localization features; based on sorting signals, amino acid composition and functional motifs. After conversion, a simple k-nearest neighbor classifier is used for prediction. To predict the subcellular localization of your target protein, simply paste your protein's amino acid sequence (single letter code) in the WoLF PSORT window below and click submit.

DeepLoc - 2.0

Prediction of eukaryotic protein subcellular localization using deep learning. DeepLoc 2.0 predicts the subcellular localization(s) of eukaryotic proteins. DeepLoc 2.0 is a multi-label predictor, which means that is able to predict one or more localizations for any given protein. It can differentiate between 10 different localizations: Nucleus, Cytoplasm, Extracellular, Mitochondrion, Cell membrane, Endoplasmic reticulum, Chloroplast, Golgi apparatus, Lysosome/Vacuole and Peroxisome. Additionally, DeepLoc 2.0 can predict the presence of the sorting signal(s) that had an influence on the prediction of the subcellular localization(s).

MembraneFold

About MembraneFold

MembraneFold combines two types of protein sequence prediction tools: protein structure (AlphaFold  [1] and OmegaFold [2] and transmembrane protein topology (DeepTMHMM [3]. The Mol* toolkit [4] is used for visualisation.

The purpose of MembraneFold is to present membrane positioning and structure predictions of a given protein chain simultaneously. The tool allows to obtain a fast overview of this information and quickly toggle between the topology annotation and the structure confidence scores.

sorry it took me so long to get to this ask!

this is really neat, and i think its great to see more tools predicting what happens to certain structures. i did consider looking for localization signals in the proteins i am making for this blog, but ultimately decided against it to keep things easier for me. furthermore, i honestly don't entirely trust most of these to even make it through the translation step, and i shudder to think what a mess any sort of co-localization would make on top of the existing horror of my abominations. to be honest i'm also just not sure how to use these and don't really want to download any more software, at least not until i have more free time. however, its still really fun to mess around with tools like this, and i highly encourage anyone interested to look into it!

letter sequence in this ask matching protein-coding amino acids:

WLFPSRTisanetensinfthePSRTIIprgramfrprteinscelllarlcaliatinpredictinwhichisasednthePSRTprincipleWLFPSRTcnvertsaprteinsaminacidseqencesintnmericallcaliatinfeatresasednsrtingsignalsaminacidcmpsitinandfnctinalmtifsAftercnversinasimpleknearestneighrclassifierissedfrpredictinTpredictthescelllarlcaliatinfyrtargetprteinsimplypasteyrprteinsaminacidseqencesinglelettercdeintheWLFPSRTwindwelwandclicksmitDeepLcPredictinfekaryticprteinscelllarlcaliatinsingdeeplearningDeepLcpredictsthescelllarlcaliatinsfekaryticprteinsDeepLcisamltilaelpredictrwhichmeansthatisaletpredictnermrelcaliatinsfranygivenprteinItcandifferentiateetweendifferentlcaliatinsNclesCytplasmEtracelllarMitchndrinCellmemraneEndplasmicreticlmChlrplastGlgiapparatsLyssmeVacleandPerismeAdditinallyDeepLccanpredictthepresencefthesrtingsignalsthathadaninflencenthepredictinfthescelllarlcaliatinsMemraneFldAtMemraneFldMemraneFldcminestwtypesfprteinseqencepredictintlsprteinstrctreAlphaFldandmegaFldandtransmemraneprteintplgyDeepTMHMMTheMltlkitissedfrvisalisatinTheprpsefMemraneFldistpresentmemranepsitiningandstrctrepredictinsfagivenprteinchainsimltaneslyThetlallwsttainafastverviewfthisinfrmatinandqicklytggleetweenthetplgyanntatinandthestrctrecnfidencescres

protein guy analysis:

this one doesn't look great, with lots of loops that do not seem to stick together and are just floating loosely and horribly around the outside of the protein. while none of this is predicted with much confidence, the middle does look slightly better. it is made up of several alpha helices arranged in a way that almost resembles a protein channel if i don't think too hard about it and am blindingly optimistic.

predicted protein structure:

[jcsmicasereports]

Acute kidney injury following exposure to a formaldehyde –free hair straightening products by Dr. Nabil Abu-Amer in Journal of Clinical Case Reports Medical Images and Health Sciences

ABSTRACT

Formaldehyde- free hair straightening products are hair smoothening solutions widely used by professional beauty salons. Formaldehyde-free hair straighteners do not technically contain formaldehyde, however they contain other chemicals such as glyoxyloyl carbocysteine which releases formaldehyde upon contact with heat. Moreover, its by-product glyoxylate may convert to oxalate, both compounds have potential nephrotoxic effect.

Case presentation: 41-year-old woman presented to the emergency room with weakness, nausea , vomiting and  stage three acute kidney injury according to Kidney Disease: Improving Global Outcomes acute kidney injury staging (KDIGO) shortly after exposure to formaldehyde - free hair straightening product, other causes of acute kidney injury were excluded such as preceding acute illness, drug history or others nephrotoxic agent exposure On physical examination the patient was pale, her vital signs were normal. The urine microscopy and serologic workup was not indicative. Kidney core biopsy reveal interstitial edema, acute interstitial nephritis and oxalate crystal nephropathy. Kidney function completely recovered after a short course of steroid therapy.

Conclusions: We present a case of severe kidney injury after exposure to hair straightening products branded as formaldehyde free but actually contain other chemicals products which release formaldehyde and other toxic chemicals when heated during the straightening procedure and  may cause systemic toxicity, particularly kidney injury. Different cosmetic products are widely in use, not all are under a tight regulation, and therefore it is important to raise the awareness of both medical teams and consumers of possible adverse health effects of different cosmetic products.

INTRODUCTION

Nephrotoxicity is defined as kidney injury due to toxic effects of chemicals. There are various forms of chemicals and drugs that may affect renal function in various mechanism including acute tubular necrosis (ATN), tubulopathy and electrolyte imbalance, acute interstitial nephritis (AIN), glomerular damage, crystal nephropathy, and thrombotic microangiopathy [1-3].

Formaldehyde- free hair straightening products contain potentially toxic chemicals other than formaldehyde. One potential such substance is glyoxyloyl carbocysteine, which is composed of glyoxylic acid, cysteine and acetic acid. Glyoxylic acid both releases formaldehyde when heated and is converted into either glycine by AGT1 (alanine:glyoxylate aminotransferase 1) or oxalate by glycolate oxidase in the human cell peroxisomes [4].

Formaldehyde is a colorless aldehyde poisonous gas at room temperature [5]. It is usually mixed with water and when the small fraction of soluble formaldehyde reacts with water, it quickly forms methylene glycol. For every molecule of free formaldehyde, 1,820 molecules of methylene glycol are formed [6]. Methylene glycol reverts back to free formaldehyde almost immediately upon contact with air or skin. Formaldehyde is thus absorbed through skin, eyes, and inhalation, and is eliminated through the urine [7-8]. During the hair straightening process, high levels of formaldehyde are found in samples of air taken from beauty salons [9] and in specimens of hairstylist workers skin [10-11].

In the kidney, formaldehyde has been reported to cause direct cytotoxic effect resulting in acute toxic tubular necrosis [12-13], and may also cause an immune system response leading to acute interstitial nephritis.

Another potential nephrotoxic component of hair straightening products is oxalate, which is an end product of glyoxylic acid.  Increased levels of oxalate promote calcium oxalate precipitation in various tissues including the kidneys, resulting in toxic injury.

Case presentation

A 41-year-old woman with a history of hypothyroidism and sleeve gastrectomy five years ago, presented to the emergency department with profound weakness, nausea and vomiting. Her symptoms began three days earlier, immediately after using a professional hair straightening formaldehyde- free product in a professional beauty salon.

On physical examination the patient was pale, her vital signs were normal, heart rate  was 66 bpm, blood pressure was 125/70 mmHg, she had no fever or respiratory distress and appeared euvolemic.

Laboratory investigations revealed a serum creatinine of 3.46 mg/dl (one year prior to the event Cr. value was 0.6 mg/dl), urea 77 mg/dl, and electrolytes, liver function tests, Beta human chorionic gonadotropin (β-hCG) and complete blood count were normal. Blood venous gases revealed: pH 7.375, HCO3 21 mmol/L and base excess 3 mmol. The anion gap and serum osmolar gap were normal. Urinalysis demonstrated leukocyturia +1 without hematuria or proteinuria.

During hospitalization urine output was normal, repeat urinalysis demonstrated leukocyturia +1 without hematuria or proteinuria, and Bence-Jones protein was negative. Urine microscopy demonstrated epithelial cells with few white blood cells without any casts or crystals. Renal ultrasound showed 14.4 cm bilateral echogenic, edematous renal parenchyma (shown in  Fig. 1).

A full serologic workup including hepatitis B and C, Human immunodeficiency virus (HIV), syphilis, antinuclear antibody (ANA) , Anti-double stranded DNA, Antineutrophil cytoplasmic antibody (ANCA), Anti-Phospolipid antibody (APLA) was normal except for a complement C3 level of 80 mg/dl (normal range 90-110 mg/dl).

On the 4th hospitalization day a renal core biopsy was performed. The histologic examination (shown in Fig. 2) was correlatd with  acute tubular necrosis, tubulo- intersitial nephritis and oxalate crystals . With the diagnosis of interstitial nephritis, the patient was started on prednisolone 1 mg/kg, one week later serum creatinine decreased to a level of 0.98 mg/dl.

A: Glomeruli were normo-cellular and without signs of active glomerular disease (arrow heads), tubules showed signs of diffuse tubular injury (black arrow) and tubules contained oxalate crystals (blue arrow). B:The interstitium showed edema associated with multifocal mixed inflammatory infiltration with multiple eosinophils and foci of tubulitis. C:There was one epithelioid granuloma. D:Tubules contained oxalate crystals (blue arrow) observed under polarized light-microscopy. Immunofluorescence analysis revealed C3 1+ in blood vessel walls only.

Discussion

This patient presents an unusual case of kidney toxic and inflammatory injury accompanied with oxalate deposition secondary to hair straightening product. In a literature review, only few cases [14-15] of acute kidney injury (AKI) following hair straightening formaldehyde- free product exposure were reported. All cases were reported after 2019. The spectrum of kidney injury following hair straightening ranges from mild to severe kidney injury requiring renal replacement therapy. The histopathologic changes reported mainly depicted severe acute tubular necrosis and acute interstitial nephritis.

Our patient presented with stage 3 AKI following hair straightening formaldehyde - free product exposure. Other causes of AKI were excluded such as preceding acute illness, drug history or other nephrotoxic agent exposure. Laboratory workup revealed leukocyturia +1, and ultrasonography was significant for enlarged edematous echogenic renal parenchyma. Kidney biopsy demonstrated acute interstitial nephritis, oxalate crystal precipitation and acute tubular necrosis. We speculate that the clinical presentation and the histopathologic changes directly resulted from exposure to the hair straightening formaldehyde- free product.

In reviewing the ingredients of the specific product used in this case, it included glyoxyloyl carbocysteine, glyoxyloyl keratin amino acid, propylene glycol glycerin, phenoxyethanol, ethylhexylglycerin disodium and other collagen, surfactant and fragrance components. We did not find evidence in the medical, pharmacological and chemical literature that any of these substances causes acute kidney injury other than glyoxyloyl carbocysteine.

Many hair straightening products are labeled as formaldehyde "free" but actually contain chemicals such as glyoxyloyl carbocysteine or methylene glycol which release formaldehyde and other toxic chemicals when heated, e.g the carbocysteine hair treatment represents the combination of glyoxylic acid + cisteine + acetic acid. Glyoxylic acid contains an aldehyde functional group, glyoxylic acid behaves as an aldehyde by  heating during the hair straightening process thus releasing high levels of formaldehyde gas exceeding the capacity of exposure[16]. On top of that, glyoxylic acid absorbed through the scalp may had converted to oxalic acid [17] which may precipitate in kidney tissue. It is possible that other components such as propylene glycol may cause osmotic renal injury. In this case, serum osmotic gap was not available since it calculated four days after exposure.

Conclusion

In conclusion, a case of severe kidney injury after exposure to hair straightening products branded as formaldehyde free is presented. This case highlights the sensitivity of the kidney to various environmental and commercial products, some of which have not been fully characterized or identified yet.

It is important to raise the awareness of both medical teams and consumers, of possible adverse health effects of different cosmetic products, including acute kidney injury, and perhaps promote tighter regulation of such products.

Statement of Ethics:

Ethical approval is not required for this study in accordance with local or national guidelines.

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available.

Conflict of Interest interests

The authors have no conflict of interest to disclose

Funding

No funding was obtained for this study.

Authors’ contributions

NAA, NZ, SM, PB, were involved in the clinical management of the patient.

NAA, MK, collected the data and wrote the first version of the manuscript.

NAA, NZ, MK, SM, PB approved the final version of the manuscript.

The authors read and approved the final manuscript.

Data Availability

All data that support the findings of this study are included in this article.

[blueoaknx]

Reclaim Vitality: The Science Behind Mitochondrial Biogenesis

Mitochondrial biogenesis is the cellular process of increasing the number of mitochondria, the organelles responsible for generating energy. This process is essential for maintaining cellular health and vitality, particularly in tissues with high energy demands, such as muscles. Mitochondrial biogenesis is often triggered by increased energy demand, usually resulting from exercise, caloric restriction, or the intake of specific nutrients.

Mitochondria are the energy producers of the cell, generating ATP, the energy currency of the cell, through oxidative phosphorylation. As cells face greater energy demands, they need more mitochondria to meet these requirements efficiently. The increase in mitochondrial numbers allows cells to produce more energy and better adapt to stress, thus enhancing overall health, recovery, and performance.

Key Factors Involved in Mitochondrial Biogenesis

Several molecular regulators drive mitochondrial biogenesis, with the most important being:

PGC-1α ActivationPGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha) is recognized as the master regulator of mitochondrial biogenesis. This protein plays a pivotal role in controlling the transcription of nuclear genes that encode mitochondrial proteins. When activated by external stimuli like exercise, PGC-1α interacts with transcription factors like NRF-1 and NRF-2 to drive the production of new mitochondria. This results in increased mitochondrial DNA (mtDNA) replication and the synthesis of mitochondrial proteins necessary for energy production and cellular respiration.

AMPK & SirtuinsAMPK (AMP-activated protein kinase) is another critical regulator that responds to low energy levels within the cell (a high AMP ratio). It activates PGC-1α, which, in turn, increases the number of mitochondria. AMPK is activated during energy-demanding activities such as endurance exercise and fasting. Sirtuins (SIRT1) are a class of NAD+-dependent enzymes that also regulate mitochondrial biogenesis. Sirtuins, especially SIRT1, deacetylate PGC-1α, further activating it to promote the transcription of mitochondrial genes. Both AMPK and sirtuins respond to energy deprivation, whether through physical exertion or caloric restriction, helping cells increase energy efficiency and prolong cellular longevity.

Antioxidant Defense and Cellular ResilienceOne of the benefits of mitochondrial biogenesis is the enhancement of cellular resilience through improved antioxidant defences. Mitochondria are not only energy producers but also sources of reactive oxygen species (ROS), which can damage cells if not adequately managed. By increasing the number of healthy mitochondria, cells improve their ability to manage oxidative stress. New mitochondria are typically more efficient at energy production and less likely to produce excess ROS, reducing overall cellular damage. This process helps to protect cells from age-related decline and stress-induced damage.

How Mitochondrial Biogenesis Impacts Health and Performance

Mitochondrial biogenesis is essential for maintaining optimal energy production, particularly during periods of increased physical activity or stress. In muscle cells, the increased number of mitochondria leads to improved ATP generation, enhancing endurance and reducing fatigue during prolonged exercise. This is particularly important for athletes or individuals who engage in regular physical activity, as their muscles require a constant supply of energy for performance and recovery.

For general health, mitochondrial biogenesis supports metabolic efficiency and longevity. In metabolic disorders like type 2 diabetes and obesity, mitochondrial dysfunction often results in impaired energy metabolism and increased oxidative stress. By promoting mitochondrial biogenesis, cells can restore normal mitochondrial function, improving insulin sensitivity and energy balance. Furthermore, mitochondrial biogenesis may help reduce the risk of chronic diseases related to ageing by maintaining cellular energy production and reducing oxidative stress.

Beyond exercise and metabolic health, mitochondrial biogenesis is also a key factor in the body’s ability to adapt to various stressors, whether environmental or nutritional. The increase in mitochondrial capacity allows cells to better handle changes in energy demand, supporting recovery and cellular adaptation. For instance, during periods of caloric restriction, mitochondrial biogenesis helps the body use energy more efficiently, contributing to longer-term health benefits, including improved longevity and resistance to age-related diseases.

Supporting Mitochondrial Biogenesis with Nutraceuticals

In addition to lifestyle factors like exercise and caloric restriction, certain nutraceuticals can support mitochondrial biogenesis. Mitokatlyst™-E is one such product that targets mitochondrial function, optimising energy production, and promoting muscle recovery. By stimulating the molecular pathways involved in mitochondrial biogenesis, such products can enhance the body’s ability to adapt to stress, recover more efficiently, and improve overall cellular function.

Conclusion

Mitochondrial biogenesis is a vital process that supports energy production, cellular health, and adaptability to environmental and physical stressors. By regulating pathways such as PGC-1α, AMPK, and sirtuins, cells can increase mitochondrial content to meet higher energy demands, promote muscle recovery, and improve overall vitality. Products like Mitokatlyst™-E are designed to optimise mitochondrial function, helping the body adapt to stress and maintain optimal cellular health. By supporting mitochondrial biogenesis, we can improve energy efficiency, enhance physical performance, and promote long-term health and resilience.

[castingcomets]

In my senior year of highschool we had a final project in AP Biology which was open-ended and could be just about anything. I rewrote (and performed) Thrift Shop to be about various branches of biology using the terminology that we had used that year. I titled it "Niche Shop."

These are the lyrics.

^ So you can follow along.

Hey… You wanna go niche shopping?

I’m an organism I’m alive You can tell by how all my cells utilize I’m- I’m- I’m growing, adapting and I’m showing, This is my response

Walk into a niche like what up I’m an organism Organ cells, organelles, carbon-based organ systems If I’m surviving, got the traits you wanna copy Got ‘em like- “Damn, I better acquire mimicry”

Factor in, fitness my kin Nat select me as a king Dressed as a warning or I’m camouflaged from everything The strongest or the fastest, sharper than Damascus But if you really wanna live, you gotta have looooong… Telomeres!

Hoofin’ it, wingin’ it, gonna optimal forage it Passin’ up through the TD forest Humus is a freebie nourish Not rockin’ semelparity but, I am a rarity 1.8 meters too much room for a disparity!

An issue of polarity, Irregularity of molarity, Disrupts cellular activity Lacking biologic dexterity

Dehydration synthesis, poly or di Covalent bonding with all the mama-saccharides!

They had an H ion, I took an H ion For ETC so I can have the energy to hang on Mito makes a maze of its membranes To gain energy used in transduction signal pathway chains

I could take some bases, Rough ‘em up and misplace The wild types would be like “Oh, he got the lactase”

I’m gonna eat some carbs I need energy and I’m on guard I’m- I’m- I’m drinking, drying and I’m linking, This is glycosidic

I’m gonna bond some peptides There are four structures so please stay wise I’m- I’m- I’m asking, amino group and acid, But don’t forget nucleotides (AUOHW!!)

What’chu know about being hydrophobic? What’chu know about being hydrophilic? I’m diffusion’, I’m movin’ right through that fatty bilayer Meet the mosaic and all its necessary players!

Thank Aunt Ester, for linking glycerols and fatty acids It’s an asset keep ‘em like molasses Metabolism, you can have in catabolic (bolic) Minus delta G or you can have it anabolic (bolic)

Prokaryotes, no nucleus All have membranes like eukaryotes Cyto-structure and ribosomes and DNA in that cytoplasm Eukaryotes have organelles in that cytoplasm Lysosomes and vacuoles in that cytoplasm

They’re like “oh, that peroxisome, that’s hella tight” I’m like “yo… that makes hydrogen peroxide” Competitive inhibition will render us quickly illin’ Catalyse that catalase to cure our condition

Don’t forget, ‘bout the mosaic composition Don’t forget, about what lets somethin’ else in That receptor is hella though But havin’ a common one in a pandemic is a hella NO

Peep gang, come take a look at my DNA Find all the nights I spent with retroviral RNA

[Interlude] In your DNA … viral RNA … turned to DNA … and then to RNA Immune … poppin’ cells … yeah!

I’m gonna place some tags Ubiquitin be quittin’ on all these proteins This cellular machine, RNA in vaccines An acid for every codon

I made God to be in my image All these kids descend from my lineage I have eternal DNA My fitness is secured through advantageous traits [X2]

As DNA replicates Every cell from a cell - this never dates I’m- I’m- I’m growing, adapting and I’m showing, This is my response

Are those your Grandpa’s genes?

[professorthick]

Hey, so I read your ask on that other blog about adiponectin and how it basically converts fat from visceral to subcutaneous. Do you know if there's any supplements or medicaments one could take to increase adiponectin levels? purely hypothetically, of course.

Yes, MCT oil boosts adiponectin levels. See these studies for more info:

Lower weight gain and higher expression and blood levels of adiponectin in rats fed medium-chain TAG compared with long-chain TAG

Medium Chain Fatty Acids Are Selective Peroxisome Proliferator Activated Receptor (PPAR) γ Activators and Pan-PPAR Partial Agonists

Genetic modulation of PPARgamma phosphorylation regulates insulin sensitivity

[farcillesbian]

I'm drawing a cell diagram so I have my own image to use for presentations and stuff. but I'm having trouble picking colours for all the organelles. so I would like to task you - mutuals, followers, maybe even mutuals in law if someone decides to reblog this.. anyone who sees this - with suggesting colours for the organelles I have left!

here's what I have currently:

[id: an in-progress drawing of a cell with pale periwinkle cytoplasm, a pink rough endoplasmic reticulum with red ribosomes, a light yellow nucleus with blue-green nucleolus, and a few orange mitochondria. /end id]

the organelles that I need colours for are:

1. smooth endoplasmic reticulum (like rough ER but no dots - should I make it same colour??)

2. lysosome (small orb)

3. peroxisome (medium orb)

4. Golgi apparatus (silly looking blob guys)

5. vacuole (lone blobs)

6. centrosome (orb with tiny orbs)

if your favourite organelle isn't here feel free to suggest it with a colour and maybe I'll add it!

[whats-in-a-sentence]

Carbon, nitrogen, and oxygen atoms circulate through photorespiration (Figure 8.9). (...) These cycles are interlocked with the photosynthetic electron transport system for the supply of ATP and reducing equivalents (reduced ferredoxin and NADPH) (see Figure 8.9).

"Plant Physiology and Development" int'l 6e - Taiz, L., Zeiger, E., Møller, I.M., Murphy, A.

[jobrxiv]

Graduate Student in Retinal Biology University of Alberta See the full job description on jobRxiv: https://jobrxiv.org/job/university-of-alberta-27778-graduate-student-in-retinal-biology/?feed_id=89461 #induced_pluripotent_stem_cells #lipids #mammalian_cell_culture #peroxisome #retina #ScienceJobs #hiring #research

[twinkl22004]

“Severe Obesity”, Victor McKusick, Mendelian Inheritance in Man, 1966. 过氧化物酶体增殖剂激活受体 (PPARG).

Here I present: “Severe Obesity”, Victor McKusick, Mendelian Inheritance in Man’, 1966. 过氧化物酶体增殖剂激活受体 (PPARG). INTRODUCTION. Severe obesity is predominantly a polygenic and multifactorial trait. Genetic variation in some genes have been associated with susceptibility to obesity as a monogenic trait of BMI. Peroxisome proliferator–activated receptors (PPAR) are a group of nuclear…