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  #1   ^
Old Thu, Apr-23-09, 16:59
Valtor's Avatar
Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Progress: 58%
Location: Québec, Canada
Default The Adiponectin thread...

I Wish I could rename the title of this thread to The Adiponectin thread.

Quote:
Adiponectin is a protein hormone that modulates a number of metabolic processes, including glucose regulation and fatty acid catabolism. Adiponectin is exclusively secreted from adipose tissue into the bloodstream and is very abundant in plasma relative to many hormones. Levels of the hormone are inversely correlated with body fat percentage in adults, while the association in infants and young children is more unclear. The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis, non-alcoholic fatty liver disease (NAFLD) and an independent risk factor for metabolic syndrome.

Quote:
Supplementation by differing forms of adiponectin were able to improve insulin control, blood glucose and triglyceride levels in mouse models.

Code:
Adiponectin affects: * glucose flux o gluconeogenesis o glucose uptake * lipid catabolism o β-oxidation o triglyceride clearance * protection from endothelial dysfunction (important facet of atherosclerotic formation) * insulin sensitivity * weight loss * control of energy metabolism.

Quote:
Because adiponectin is a novel hormone, no therapy has yet been developed with adiponectin and it may be some years before clinical trials commence. One obvious pharmaceutical treatment would be the administration of adiponectin; in mouse models such administration has shown positive effects.

http://en.wikipedia.org/wiki/Adiponectin

Quote:
Adiponectin can cause weight loss by raising metabolic rate while not affecting appetite

Quote:
When adiponectin, which is involved in glucose and lipid metabolism, was introduced into the cerebrospinal fluid of normal mice, they showed no changes in food intake, but their metabolism rose. "The animal burns off more calories, so over time loses weight, which was very fascinating because we knew that leptin caused weight loss by suppressing appetite and increasing metabolic rate," explains [lead author Rexford] Ahima. "Here we have another fat hormone that can cause weight loss but without affecting intake."

http://scienceandreason.blogspot.co...diponectin.html

Quote:
However, this new study shows that there is something else involved — exercise helps us shed belly fat because it increases the production of adiponectin.

Quote:
Adiponectin is a hormone produced in fat cells that increases the effectiveness of insulin. Studies show when we have plenty of adiponectin, not only is our insulin production lower, our blood sugar is better controlled, and that decreases our risk of diabetes and heart disease.

Quote:
However, when we gain weight, adiponectin production goes down. Weight that is gained in the belly, as opposed to weight gained more in the hips and thighs, is the weight that dramatically reduces adiponectin production. So, as you gain weight and adiponectin production drops, your weight just gets worse.
Quote:
But now we know that a way to get that adiponectin back up is through exercise! In the study, brisk walking mixed with light jogging 4-5 days per week for 40 minutes per session increased adiponectin in adult overweight males. Adiponectin levels rose 260% after two to three bouts of exercise despite unchanged body weight, and even remained elevated after 10 weeks.

http://www.totalhealthbreakthroughs...onectin-rising/

Quote:
The circadian clock controls energy homeostasis by regulating circadian expression and/or activity of enzymes involved in metabolism. Disruption of circadian rhythms may lead to obesity and metabolic disorders. We tested whether the biological clock controls adiponectin signaling pathway in the liver and whether fasting and/or high-fat (HF) diet affects this control. Mice were fed low-fat or HF diet and fasted on the last day. The circadian expression of clock genes and components of adiponectin metabolic pathway in the liver was tested at the RNA, protein, or enzyme activity level. In addition, serum levels of glucose, adiponectin, and insulin were measured. Under low-fat diet, adiponectin signaling pathway components exhibited circadian rhythmicity. However, fasting and HF diet altered this circadian expression; fasting resulted in a phase advance, and HF diet caused a phase delay. In addition, adenosine monophosphate-activated protein kinase levels were high during fasting and low during HF diet. Changes in the phase and daily rhythm of clock genes and components of adiponectin signaling pathway as a result of HF diet may lead to obesity and may explain the disruption of other clock-controlled output systems, such as blood pressure and sleep/wake cycle, usually associated with metabolic disorders.

High-Fat Diet Delays and Fasting Advances the Circadian Expression of Adiponectin Signaling Components in Mouse Liver

This would all fit with Pennington's hypothesis: http://forum.lowcarber.org/showthread.php?t=394699

I'm currently testing this. I made a mix of dried potato powder and whey & egg protein powder (vanilla flavor and stevia sweetened). I make it so there is 70g carbs and 90g proteins, which are my Dr K. ratios. Then I add boiling water to it until it reaches the texture of mashed potatoes. That's my food for an entire day.

Plus I continue taking my supplements.

- Vitamin D3 5000iu/d
- Magnesium 300mg/d
- Omega (swiss labs) 2400mg/d
- B 100 complex/d
- The Right C 1000mg/d
- Norwegian Kelp 1500mg/d (1.5 mg iodine)
- Maca pills (don't remember amount)
- Glucosamine Sulfate 3000mg/d

Patrick

Last edited by Valtor : Thu, Apr-23-09 at 20:41.
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  #2   ^
Old Thu, Apr-23-09, 17:03
Valtor's Avatar
Valtor Valtor is offline
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Plan: VLC 4 days a week
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Default

Quote:
Under fasting, low levels of adenosine monophosphate (AMP) activate the expression of AMP-activated protein kinase (AMPK) leading to the phosphorylation of casein kinase I epsilon (CKIε). Phosphorylated CKIε leads to the degradation of PER proteins generating a phase advance (47). High-fat diet lowers the levels of activated AMPK, CKIε remains in the hypo-phosphorylated state and the half-life of the PER proteins increases, which leads to a phase delay.

http://endo.endojournals.org/cgi/da...2008-0944/DC1/3
http://endo.endojournals.org/cgi/co...n.2008-0944/DC1

Patrick
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  #3   ^
Old Thu, Apr-23-09, 17:08
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Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Quote:
Researchers in Israel have observed a link between a high fat diet and disruption to circadian rhythms in mice, which could have a bearing on metabolic disorders.

Circadian rhythms are the body’s ‘clock’ that regulates expression and activity of enzymes and hormones involved in metabolism The researchers at The Hebrew University of Israel noted that disruption of the circadian rhythms may lead to obesity and metabolic disorders. Such disorders may include hormone imbalance, psychological and sleep disorders, some forms of cancer, and obesity.

The study findings, if relevant to humans, would show a cause and effect relation between diet and biological clock imbalance.

Dr Oren Froy and colleagues from the Institute of Biochemistry, Food Science and Nutrition set out to uncover whether the biological clock controls the adiponectin signaling pathway in the liver of mice. Adiponectin is a protein hormone that is involves in glucose and fat metabolism, and is secreted from fat tissues known as adipocytes.

They wanted to know whether this control is affected by fasting and/or a high fat diet in a mouse model.

The experiments showed that “under low-fat diet, adiponectin signaling component pathways exhibited circadian rhythmicity”. However they noted that this circadian expression was altered by both fasting and a high fat diet.

In the case of fasting, phases were advanced; with the high fat diet, they were they were delayed.

In addition, levels of adenosine monophosphate-activated protein kinase (a protein involved in fatty acid metabolism) were high during fasting and low during the high fat diet.

“Changes in the phase and daily rhythm of clock genes and components of adiponextin signaling pathways as a result of HF diet may lead to obesity and may explain the disruption of other clock-controlled output systems, such as blood pressure and sleep/wake cycle, usually associated with metabolic disorders,” wrote Froy and collegues.

Methodology

The study involved feeding mice either a low-fat diet or a high-fat diet, then put them on a one-day fast. They then measured components of the adiponectin metabolic pathway at the RNA, protein and enzyme activity level, as well as serum levels of glucose, adiponectin and insulin.

http://www.nutraingredients.com/Res...lock-disruption

Patrick
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  #4   ^
Old Thu, Apr-23-09, 17:16
Valtor's Avatar
Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Location: Québec, Canada
Default

Contradictory...

I believe they were just wrongly correlating. We have seen this with other studies in nutrition.

Quote:
Insulin Sensitizer Also Serves As Energy-conserving Signal To The Brain (7/12/07)
A fat-derived protein known for its effects on the liver and skeletal muscle might also serve as an energy-conserving signal to the brain during periods of starvation, suggests a new study in the July issue of Cell Metabolism, a publication of Cell Press. The substance, known as adiponectin, acts on the brain to boost appetite and slow energy expenditure in an effort to maintain adequate fat stores during lean times, the researchers report.

First off, there is the question of whether adiponectin even reaches the central nervous system.
The researchers now report evidence in mice that adiponectin receptors are present in the hypothalamic region of the brain and that some forms of the chemical enter the cerebrospinal fluid from the blood.

Then, supposing adiponectin reaches the central nervous system, there is the question of what effect, if any, it has there.
Once in the brain, adiponectin enhances the activity of a metabolic enzyme called AMP-activated protein kinase (AMPK) to stimulate greater food consumption.

Moreover, the researchers found that adiponectin decreased energy expenditure. They also showed that blood and spinal fluid adiponectin levels in the brain normally increase during fasting and decrease after refeeding, suggesting that adiponectin acts mainly during food shortages.

So this research claims that adiponectin increases appetite, unlike leptin, which has the opposite effect. Further, adiponectin leads to lower activity and energy expenditure, thus conserving available energy supplies. But such effects are reversed if adiponectin is absent:
In adiponectin-deficient mice, AMPK activity in the brain slowed, causing the animals to eat less and expend more energy. That action, in turn, made the animals resistant to becoming obese even on a high-fat diet. Moreover, animals lacking adiponectin lost more fat after 12 hours of fasting than normal mice did.

If indeed adiponectin tends to lead to lower activity levels and energy expenditure, one has to ask whether it promotes fat storage or even obesity.

http://scienceandreason.blogspot.co...diponectin.html

Patrick

Last edited by Valtor : Thu, Apr-23-09 at 18:00.
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  #5   ^
Old Thu, Apr-23-09, 17:31
lil' annie lil' annie is offline
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Plan: quasi paleo + starch
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This is really fascinating, and it provides interesting confirmation of Dr. Jan Kwasniewski's dietary ratios for the obese, where the protein/fat becomes equal: 1:1, and I believe that the carbs were '0.50.'
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  #6   ^
Old Thu, Apr-23-09, 17:37
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Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
BF:
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Location: Québec, Canada
Default

Humm, that would mean I should be using 45g of carbs. Where did you get these ratios ?

Patrick
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  #7   ^
Old Thu, Apr-23-09, 17:52
lil' annie lil' annie is offline
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Plan: quasi paleo + starch
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Quote:
Originally Posted by Valtor
Humm, that would mean I should be using 45g of carbs. Where did you get these ratios ?

Patrick



I saw them online several days ago, and then again today, when Pangolina - who actually owns the books, and who has actually read the books, and who actually has firsthand personal experience following Dr. JK's Homo Optimal Diet program - she mentioned the same ratios that I read about for obese persons -- the ratios are different for overweight people, and again different for normal weight people -- individuals who've been following the H.O.D. for a long time and have no need to lose any weight frequently use 1:5:1 as their longterm maintenance ratios.

You might want to carefully read all of Pangolina's postings - there aren't dozens & dozens, not by any stretch of the imagination - I'm sure you could read everything she's posted here, in no time at all.

For her discussion of the ratios above, which I have read elsewhere, too, online, please go to page 10 of this thread:


Paleo Critique of the Optimal Diet
Paleolithic & Neanderthin Forum
Active Low-Carber Forums


http://forum.lowcarber.org/showthre...47&page=1&pp=15


Quote:
Originally Posted by pangolina


This isn't necessarily true; as you've said yourself, it takes some time for the body to be willing to give up its fat stores. This can happen very quickly for some, and more slowly for others.


For an overweight person, it can indeed stay at 1:2.5 for the whole time, if that's what works best for them. It really depends on their body, and the degree of overweight.

For an obese person, the fat intake can go very low, once rapid weight loss has begun. Then it goes up to 1:2.5 once they've lost most of the weight (and are thus "overweight" rather than obese). Then up to 1:3.5 for maintenance, and even 1:4 or 1:5 for a very fit person with high energy needs.


Then I guess Dr. Kwasniewski doesn't, either.


Thank you for the suggestion. I take it that this means that you're no longer promoting the Optimal Diet. If not, I hope you'll at least take a break until you've familiarized yourself with some more of Dr. Kwasniewski's work.


"Optimal Nutrition" isn't my theory; it's Jan Kwasniewski's. If you don't believe in it, that's all right with me. I'm posting for the benefit of others, who are interested in learning about what he has to say. (FWIW, a lot of the people on the Paleo forum seem to be interested in more than just weight loss.)

And I'm not distressed -- this is a logical issue, not an emotional one.


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  #8   ^
Old Thu, Apr-23-09, 17:57
KJF KJF is offline
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The major reservation I have with this is that they're giving a high fat diet to mice, who don't normally eat much fat at all. This really calls for a human trial.
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  #9   ^
Old Thu, Apr-23-09, 18:02
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Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Location: Québec, Canada
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Quote:
Originally Posted by KJF
The major reservation I have with this is that they're giving a high fat diet to mice, who don't normally eat much fat at all. This really calls for a human trial.

What I find interesting is this part: "Here we have another fat hormone that can cause weight loss but without affecting intake."

Patrick
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  #10   ^
Old Thu, Apr-23-09, 18:05
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Valtor Valtor is offline
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Posts: 2,036
 
Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Progress: 58%
Location: Québec, Canada
Default

Quote:
However, this new study shows that there is something else involved — exercise helps us shed belly fat because it increases the production of adiponectin.

Quote:
Adiponectin is a hormone produced in fat cells that increases the effectiveness of insulin. Studies show when we have plenty of adiponectin, not only is our insulin production lower, our blood sugar is better controlled, and that decreases our risk of diabetes and heart disease.

Quote:
However, when we gain weight, adiponectin production goes down. Weight that is gained in the belly, as opposed to weight gained more in the hips and thighs, is the weight that dramatically reduces adiponectin production. So, as you gain weight and adiponectin production drops, your weight just gets worse.
Quote:
But now we know that a way to get that adiponectin back up is through exercise! In the study, brisk walking mixed with light jogging 4-5 days per week for 40 minutes per session increased adiponectin in adult overweight males. Adiponectin levels rose 260% after two to three bouts of exercise despite unchanged body weight, and even remained elevated after 10 weeks.

http://www.totalhealthbreakthroughs...onectin-rising/

This would fit with Pennington's hypothesis: http://forum.lowcarber.org/showthread.php?t=394699

Patrick

Last edited by Valtor : Thu, Apr-23-09 at 18:17.
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  #11   ^
Old Thu, Apr-23-09, 18:10
lil' annie lil' annie is offline
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Posts: 1,276
 
Plan: quasi paleo + starch
Stats: 153/148/118 Female 5'4"
BF:
Progress: 14%
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Quote:
Originally Posted by Valtor


However, this new study shows that there is something else involved — exercise helps us shed belly fat because it increases the production of adiponectin.



http://www.totalhealthbreakthroughs...onectin-rising/

Patrick



Wow, this is news! Do you know whether they mention if it HAS TO BE *only* resistance exercise -- there are dozens of postings here alleging that only weight lifting gets rid of body fat.

However, Dr. Lustig, the pediatric endocrinologist who specializes in obesity said that exercise is CRUCIAL because it detoxifies the liver of fructose.

Which leads me to this question....

Patrick, are they saying anything about this kewl hormone in relation to ANYTHING whatsoever, fructose??




Thanks!!
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  #12   ^
Old Thu, Apr-23-09, 18:15
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Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
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Progress: 58%
Location: Québec, Canada
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Quote:
Originally Posted by lil' annie
Which leads me to this question....

Patrick, are they saying anything about this kewl hormone in relation to ANYTHING whatsoever, fructose??


Thanks!!

I believe fructose has it's own pathway to cause insulin resistance. But adiponectin might help.

Patrick
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  #13   ^
Old Thu, Apr-23-09, 18:17
lil' annie lil' annie is offline
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Posts: 1,276
 
Plan: quasi paleo + starch
Stats: 153/148/118 Female 5'4"
BF:
Progress: 14%
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Quote:
Originally Posted by Valtor
Humm, that would mean I should be using 45g of carbs. Where did you get these ratios ?

Patrick



Here's some more information from the other thread - I didn't realize that he felt that diabetics should use 0.50 for the carbs, too.

Here's what Pangolina posted in reply to my question:



Quote:
Originally Posted by pangolina
0.5 - 0.8 is the standard range for both normal and overweight. When he gives the "potted version" of the diet, sometimes he uses the former number, sometimes the latter.

0.8 is considered to be preferable for most of us -- even those who are somewhat overweight -- just to give a bit of a margin.

0.5 is required for diabetics, and can be helpful for others if weight loss proves difficult. It's the figure he most often recommends for obesity.

It's generally not necessary for the average person to go above 0.5, if you prefer to stay on the low end. But if you start getting leg cramps or signs of ketosis, he recommends raising the carbs by 15-20g.
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  #14   ^
Old Thu, Apr-23-09, 18:30
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Valtor Valtor is offline
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Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
BF:
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Location: Québec, Canada
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Concerning smoking...

Quote:
Overall, these studies demonstrate the novel observation that adiponectin and functional AdipoR1are expressed by lung epithelial cells, suggesting a potential autocrine and/or paracrine pathway for adiponectin to activate epithelial cells in COPD-E.

http://www.ncbi.nlm.nih.gov/sites/e...0,f1000m,isrctn

Patrick
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  #15   ^
Old Thu, Apr-23-09, 18:32
Valtor's Avatar
Valtor Valtor is offline
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Posts: 2,036
 
Plan: VLC 4 days a week
Stats: 337/258/200 Male 6' 1"
BF:
Progress: 58%
Location: Québec, Canada
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Quote:
OBJECTIVE— The aim of this study was to determine the effect of common adiponectin gene polymorphisms on dietary intervention-mediated changes in adiponectin levels and homeostasis model assessment of insulin resistance (HOMA-IR) indexes.

RESEARCH DESIGN AND METHODS— A total of 363 subjects with impaired fasting glucose (IFG) or newly diagnosed type 2 diabetes followed a dietary intervention (replacement of cooked refined rice with whole grains and an increase in vegetable intake) and regular walking for 12 weeks without any medication. Adiponectin gene single nucleotide polymorphisms (SNPs) (45, 276, and –11377) were examined in these subjects.

RESULTS— After this dietary intervention, fasting glucose levels decreased in all three SNP 45T>G genotype groups. Subjects with the SNP 45TT genotype showed increased adiponectin levels and decreased HOMA-IR indexes. Haplotype analysis revealed that homozygous carriers of the TG haplotype (45TT and 276GG) and heterozygous carriers of the TG haplotype (TG/X) showed a reduction in the HOMA-IR index after adjustment for baseline levels. Significant differences were observed in changes in HOMA-IR indexes and adiponectin concentrations according to the 45-276 TG haplotype in overweight-obese, but not in normal-weight subjects: the greatest decrease in HOMA-IR indexes and the greatest increase in adiponectin levels were shown in overweight-obese subjects with the TG/TG haplotype.

CONCLUSIONS— ADIPOQ genetic variants can affect circulating adiponectin levels and insulin resistance indexes in subjects with IFG or newly diagnosed type 2 diabetes in response to dietary intervention.
http://care.diabetesjournals.org/cg...stract/32/4/552

Patrick
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