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Effects of 2 types of hypoenergetic diets on hormone levels and gene expression

J Clin Endocrinol Metab. 2008 Nov;93(11):4315-22

CONTEXT: Hypoenergetic diets are used to reduce body fat mass and metabolic risk factors in obese subjects. The molecular changes in adipose tissue associated with weight loss and specifically related to the dietary composition are poorly understood.
OBJECTIVE: We investigated adipose tissue gene expression from human obese women according to energy deficit and the fat and carbohydrate content of the diet.
DESIGN AND SETTING: Obese subjects recruited among eight European clinical centers were followed up 10 wk of either a low-fat (high carbohydrate) or a moderate-fat (low carbohydrate) hypoenergetic diet.
SUBJECTS: Two sets of 47 women in each dietary arm were selected among 648 subjects matched for anthropometric and biological parameters.
MAIN OUTCOME MEASURE: We measured adipose tissue gene expression changes in one set using a candidate gene approach. The other set was used to survey 24,469 transcripts using DNA microarrays. Results were analyzed using dedicated statistical methods. Diet-sensitive regulations were confirmed on the other set of subjects.
RESULTS: The two diets induced similar weight loss and similar changes for most of the biological variables except for components of the blood lipid profile. One thousand genes were regulated by energy restriction. We validated an effect of the fat to carbohydrate ratio for five genes (FABP4, NR3C1, SIRT3, FNTA, and GABARAPL2) with increased expression during the moderate-fat diet. CONCLUSIONS: Energy restriction had a more pronounced impact on variations in human adipose tissue gene expression than macronutrient composition. The macronutrient-sensitive regulation of a subset of genes may influence adipose tissue function and metabolic response.

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This is a nice article if only to review the effects of hypocaloric diets on various hormone levels as well as cholesterol levels. There were two diets (1) a low fat, high carb diet and (2) a moderate fat low carbohydrate diet. Table 2 shows the effects of these diets on a 2o parameters including insulin, leptin, cortisol, glucose and various lipids. Both of these diets had a significant effect on many of these parameters, but the low fat diet (not surprisingly) showed a greater reduction in various lipids.

The portion of the article with regards to genetics gets rather deep and is suggested reading only for the most die-hard seekers of knowledge about obesity.

Triglycerides by fibrates not as good

Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial.

Lancet. 2005 Nov 26;366(9500):1849-61.

Keech A, Simes RJ, Barter P, Best J, Scott R, Taskinen MR, Forder P, Pillai A, Davis T, Glasziou P, Drury P, Kesäniemi YA, Sullivan D, Hunt D, Colman P, d'Emden M, Whiting M, Ehnholm C, Laakso M; FIELD study investigators.

BACKGROUND: Patients with type 2 diabetes mellitus are at increased risk of cardiovascular disease, partly owing to dyslipidaemia, which can be amenable to fibrate therapy. We designed the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study to assess the effect of fenofibrate on cardiovascular disease events in these patients. METHODS: We did a multinational, randomised controlled trial with 9795 participants aged 50-75 years, with type 2 diabetes mellitus, and not taking statin therapy at study entry. After a placebo and a fenofibrate run-in phase, we randomly assigned patients (2131 with previous cardiovascular disease and 7664 without) with a total-cholesterol concentration of 3.0-6.5 mmol/L and a total-cholesterol/HDL-cholesterol ratio of 4.0 or more or plasma triglyceride of 1.0-5.0 mmol/L to micronised fenofibrate 200 mg daily (n=4895) or matching placebo (n=4900). Our primary outcome was coronary events (coronary heart disease death or non-fatal myocardial infarction); the outcome for prespecified subgroup analyses was total cardiovascular events (the composite of cardiovascular death, myocardial infarction, stroke, and coronary and carotid revascularisation). Analysis was by intention to treat. The study was prospectively registered (number ISRCTN 64783481). FINDINGS: Vital status was confirmed on all but 22 patients. Averaged over the 5 years' study duration, similar proportions in each group discontinued study medication (10% placebo vs 11% fenofibrate) and more patients allocated placebo (17%) than fenofibrate (8%; p<0.0001) n="288)" n="256)" p="0.16)." p="0.010)" p="0.22)." p="0.035)." p="0.003)." p="0.18)." p="0.002)," p="0.0003)." p="0.031)" p="0.022),">

Atorvostatin 80 mg vs 10 mg in stable CHD. Any real benefit?

This time the full TNT study is anlayzed at Paper Shredder.

See also a shredding of the subanalysis with regards to diabetics.

Is atorvostatin 80 mg better than 10 mg for diabetics?

Check out the critical analysis at Paper Shredder.

Dyslipidemia and Diabetes