A Natural Cure for Obesity and Insulin Resistance!? Promising Results from Animal Experiments with Bitter Melon Bioactives

In a very recent investigation, researchers from the Pennington Biomedical Research Center (Wang. 2011) found that high-fat diet fed mice gained less weight and had less compromised insulin response, if they received an (unfortunately) unspecified amount of an aquaeus extract from bitter melon:

Body weight, plasma glucose, insulin, leptin levels and HOMA-IR values were significantly lower in the BM-fed HFD group when compared to the HFD group. BM supplementation significantly increased IRS-2, IR β, PI 3K and GLUT4 protein abundance in skeletal muscle, as well as phosphorylation of IRS-1, Akt1 and Akt2 when compared with HFD (P<.05 and P<.01). BM also significantly reduced muscle lipid content in the HFD mice. BM extract greatly increased glucose uptake and enhanced insulin signaling in L6 myotubes. 

There is however two major caveat to these findings. Firstly, mice ain't a particularly good model for predictions concerning the effect of supplements that are added to a high fat diet. And secondly, even if we would see similar results in human beings, the most obvious conclusion one MUST (but obviously nobody does) draw from the results of this study is that without supplementation the low fat diet, i.e. the group of mice that consumed a diet that is appropriate to their genetic make-up, gained the least amount of weight, had the lowest leptin levels and the best insulin sensitivity.

Figure 1: Insulin levels of the mice on a low fat diet (LFD), a high fat diet (HFD) and a high fat diet supplemented with bitter melon extract (BM)

Does this tell you that you should revert to a low fat diet? No, at least not if you ain't a mouse. What it should tell you, however, is that revamping your diet, making correct food choices and eating according to what our bodies are made for is the key to health and long jeopardy - the "natural cure for obesity and insulin resistance", it's already out there. Don't even think about dietary supplements before you've got that in check...

Calcium + Vitamin D for Breakfast Increase Dietarily Induced Thermogenesis and Fatty Acid Oxidation

Ever since the first studies suggested beneficial effects of dairy on weight loss, there have been a lot of trials that investigated the role of (supplemental) calcium in these contexts (mostly with discouraging results). A very recent study by Wendy and Soares (Wendy. 2011) took a very similar approach, but added vitamin D to the equation.

In their study, the scientists fed their 11 subjects (aged (mean ± SEM) 54 ± 1.2 y and BMI 31 ± 2.4 kg/m) a meal that was either high (HCT) or low (LCT) in vitamin D and calcium and measured diet induced thermogenesis (DIT), fat oxidation rates (FOR), serum leptin, subjective feelings of hunger/satiety hourly over a period of 8 hours. The results were far from earth-shattering; they could however solve the mystery of why most people find it easier to lose weight on a diet that is generally rich in dairy and calcium + vitamin D rich foods:

HCT resulted in lesser suppression of ΔFOR (p=0.02) and a significantly greater DIT (p=0.01). Further, the buffet to dinner interval was prolonged (p=0. 083) and reported 24h energy intake following this trial was significantly reduced (p=0.017). ∆leptin following HCT but not LCT was negatively related to 24 h fat intake (r = - 0.81, p=0.016).

So, the underlying mechanism is actually threefold and much different from the commonly heard hypothesis that dietary caclium would "bind fat in the intestine" and thus reduce caloric intake:

1. greater postprandial fat oxidation
2. significantly greater thermogenesis
3. beneficial effect on leptin and thus decrease in hunger

What else would you want? If there was not the issue with lactose intolerance, eating as much dairy as possible could actually become a general recommendation for everyone who intends to lose weight and/or improve body composition

Leptin & AMPK Activation in Muscle - Did Scientists Investigate the Wrong Species?

Actually, this is something I have been reminding people of for years: Human beigns are no mice and although some people may be rats, genetically they are still very different. Usually I put this argument forward if anyone presents me with a study done on rodents that "shows" how bad dietary protein, especially from meat, is for you - thin of it: when was the last time you saw a mouse eating a cow? This time the issue is a little more sophisticated, though...

Australian scientists (Laker. 2010) have recently investigated the effect of leptin on AMP-activated protein kinase (AMPK) in muscle of sheep and (I do not know if to their, but maybe to some of the proclaimed experts surprise) they found that...

[...] leptin infusion reduced (P<0.05) food intake and body weight and it also increased plasma adrenaline concentration at 6 h and 7 days, suggesting increased sympathetic nerve activity. Despite this, and in contrast to rodent studies, central leptin infusion did not increase skeletal muscle AMPKα Thr172phosphorylation or ACCβ Ser221 phosphorylation.

With sheep being genetically closer to human beings than mice, this is an interesting finding and could possible lead into new insights into why leptin, once proclaimed as possible panacea for the obesity epidemic, does work on rodents, but has little positive effect on obese human beings. Hitherto, the most accepted theory is "leptin resistance", which, similar to insulin resistance, is supposed to prevent leptin from doing its magic. This study, however, suggests that there might be genetic issues involved, as well. As always, I will keep you posted...