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| The tipping point and the metabolic syndrome. |
Fascinating stuff!
Showing posts with label Metabolism. Show all posts
Showing posts with label Metabolism. Show all posts
Tuesday, 30 April 2013
Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?
Serendipity strikes again!
The picture that I used for the last post came from Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?
Fascinating stuff!
Fascinating stuff!
Metabolic flexibility - do you have it?
I'm not quite sure what the picture below means (I need to do a spot of reading!).
While replying to Kade Storm this morning, it suddenly occurred to me that the Eskimos have an unusual ability. RER (a.k.a. RQ) normally varies from 0.7 (100% fat-burning) to 1.0 (100% carb-burning aerobically) to >1.0 (100% carb-burning, some anaerobically). Eskimos manage to get an RER of 0.600 *Mind blown.*
One theory that comes to mind is BAT. As Eskimos live in a very cold environment, it's possible that this has resulted in them having a large amount of BAT. BAT is very metabolically-active and turns ATP into heat via UCPs.
Nowadays, first-world people don't live in a cold environment (unless they're old and/or poor), so we don't have much BAT after infancy. Naturally-skinny people may be that way due to having more BAT. They seem to be able to eat whatever and as much as they want without getting fat. I'd like to scratch their eyes out! ;-)
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| Metabolic flexibility "bowl" and "Adaptability envelope" |
One theory that comes to mind is BAT. As Eskimos live in a very cold environment, it's possible that this has resulted in them having a large amount of BAT. BAT is very metabolically-active and turns ATP into heat via UCPs.
Nowadays, first-world people don't live in a cold environment (unless they're old and/or poor), so we don't have much BAT after infancy. Naturally-skinny people may be that way due to having more BAT. They seem to be able to eat whatever and as much as they want without getting fat. I'd like to scratch their eyes out! ;-)
Saturday, 23 March 2013
Everyone is Different, Part 3.
Cont'd from Everyone is Different, Part 2.
Hat-tip to Bill Lagakos, whose article Missing: 300 kilocalories reminded me of the following graphic from Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study.
Lo and behold, even when subjects are bribed to stick to the diets that they are provided with, the effect of eating those diets varies hugely.
So, people like ItsTheWoo and Petro Dobromylskyj (yes, I have to copy and paste the name from his site every freakin' time!) rave about how awful carbs are, while people like Go Kaleo and Matt Stone rave about how awesome carbs are.
Everyone is different for a number of reasons, some of which are unchangeable and some of which are changeable. We can't change our birth weight, what our mums ate when we were in the womb or the chemicals that we were exposed to in the past. We can't change our genes, but we can change the expression of our genes by changing diet, activity and even supplementation. See Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial.
Continued on Bray et al shows that a calorie *is* a calorie (where weight is concerned)
Hat-tip to Bill Lagakos, whose article Missing: 300 kilocalories reminded me of the following graphic from Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study.
Lo and behold, even when subjects are bribed to stick to the diets that they are provided with, the effect of eating those diets varies hugely.
So, people like ItsTheWoo and Petro Dobromylskyj (yes, I have to copy and paste the name from his site every freakin' time!) rave about how awful carbs are, while people like Go Kaleo and Matt Stone rave about how awesome carbs are.
Everyone is different for a number of reasons, some of which are unchangeable and some of which are changeable. We can't change our birth weight, what our mums ate when we were in the womb or the chemicals that we were exposed to in the past. We can't change our genes, but we can change the expression of our genes by changing diet, activity and even supplementation. See Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial.
Continued on Bray et al shows that a calorie *is* a calorie (where weight is concerned)
Monday, 25 June 2012
Adipocyte Hyperplasia - Good or Bad?
The answer is "It depends!".
The above plot is from Fig. 4 of Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.
As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.
If adipocytes become full due to a chronic caloric excess, there are four permutations of continued caloric excess/subsequent caloric deficit & hyperplasia/no hyperplasia.
1a: There is continued caloric excess. No preadipocytes are converted into adipocytes i.e. there is no adipocyte hyperplasia. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.
1b: There is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
2a: There is continued caloric excess. Pre-adipocytes are converted into adipocytes i.e. there is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.
2b: There is subsequent caloric deficit. Adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.
Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).
See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.
According to Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology:-
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."
If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.
The above plot is from Fig. 4 of Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.
As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.
If adipocytes become full due to a chronic caloric excess, there are four permutations of continued caloric excess/subsequent caloric deficit & hyperplasia/no hyperplasia.
1a: There is continued caloric excess. No preadipocytes are converted into adipocytes i.e. there is no adipocyte hyperplasia. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.
1b: There is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
2a: There is continued caloric excess. Pre-adipocytes are converted into adipocytes i.e. there is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.
2b: There is subsequent caloric deficit. Adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.
Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).
See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.
According to Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology:-
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."
If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.
Friday, 8 January 2010
How stuff works.
My preceding post got rather technical and delved into the finer points of cell biochemistry. For those who want to learn more about how cells work, I thoroughly recommend Metabolism at a Glance (Paperback) by Jack G Salway, Sen. Lecturer in Medical Biochemistry, University of Surrey. It's crammed with metabolic pathway diagrams.
I also recommend Medical Biochemistry at a Glance (Paperback) by Jack G Salway.
For general information on nutrition and metabolism, I recommend Introduction to Nutrition and Metabolism (Paperback) by David A Bender, Sen. Lecturer in Biochemistry, UCL.
A good site for information on fat loss, muscle gain etc is https://www.bodyrecomposition.com/.
A good site for nutrient data is https://nutritiondata.self.com/
A good site for peer-reviewed evidence is https://www.ncbi.nlm.nih.gov/pubmed/
A good site for searching textbooks is NCBI Bookshelf
A good site for clinical studies is https://clinicaltrials.gov/
A good site for enzyme structures is https://www.ebi.ac.uk/thornton-srv/databases/enzymes/.
Here's a searchable version of Biochemistry, by L Stryer.
It's a bit dry, but of interest is:-
Food Intake and Starvation Induce Metabolic Changes and
Phosphatidate Is a Common Intermediate in the Synthesis of Phospholipids and Triacylglycerols.
Here's a YouTube video of ATP Synthase, which takes a proton gradient and, using a molecular motor-generator, converts ADP + Phosphate into ATP, the energy source that cells use.
Happy reading and viewing!
I also recommend Medical Biochemistry at a Glance (Paperback) by Jack G Salway.
For general information on nutrition and metabolism, I recommend Introduction to Nutrition and Metabolism (Paperback) by David A Bender, Sen. Lecturer in Biochemistry, UCL.
A good site for information on fat loss, muscle gain etc is https://www.bodyrecomposition.com/.
A good site for nutrient data is https://nutritiondata.self.com/
A good site for peer-reviewed evidence is https://www.ncbi.nlm.nih.gov/pubmed/
A good site for searching textbooks is NCBI Bookshelf
A good site for clinical studies is https://clinicaltrials.gov/
A good site for enzyme structures is https://www.ebi.ac.uk/thornton-srv/databases/enzymes/.
Here's a searchable version of Biochemistry, by L Stryer.
It's a bit dry, but of interest is:-
Food Intake and Starvation Induce Metabolic Changes and
Phosphatidate Is a Common Intermediate in the Synthesis of Phospholipids and Triacylglycerols.
Here's a YouTube video of ATP Synthase, which takes a proton gradient and, using a molecular motor-generator, converts ADP + Phosphate into ATP, the energy source that cells use.
Happy reading and viewing!
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