Fatostatin Could Lead to Obesity Drug

[Kingcreole]

(Aug. 31) -- Scientists have discovered a small molecule, which they've named fatostatin, that stops the body from making fat.
Fatostatin could someday lead to a new all-in-one pill fighting obesity, diabetes and cholesterol.
Fatostatin blocks SREBP, which controls fat synthesis, according to Science Daily.
Obese mice injected with fatostatin in the study, published in the Aug. 28 issue of the journal Chemistry and Biology, showed noticeable weight loss without a big difference in their eating habits, the researchers found.
After four weeks, the mice weighed 12 percent less with 70 percent lower blood sugar levels, and their cholesterol levels dropped as well.
"We are frankly very excited about it," said Salih Wakil, a researcher at Baylor College of Medicine in Texas, where the study took place. "Hopefully down the road, fatostatin or a derivative of fatostatin may be helpful."


Thought this was interesting and wanted to share.

 

[Macro]

wow they found a drug (patentable) that mimics the effects of sesamin/episesamin (or at least some of them- not quite as effective or as impacting)...

1: Biochim Biophys Acta. 2001 Nov 30;1534(1):1-13. Links
Sesamin, a sesame lignan, decreases fatty acid synthesis in rat liver accompanying the down-regulation of sterol regulatory element binding protein-1.Ide T, Ashakumary L, Takahashi Y, Kushiro M, Fukuda N, Sugano M.
Laboratory of Nutrition Biochemistry, National Food Research Institute, tsukuba City, Japan. [email protected]

The effect of sesamin, one of the most abundant lignans in sesame seed, on hepatic fatty acid synthesis was examined in rats. Rats were fed experimental diets containing varying amounts (0, 0.1 and 0.2% for Exp. 1 and 0, 0.2 and 0.4% for Exp. 2, respectively) of sesamin for 15 days. The activity and gene expression of enzymes involved in fatty acid synthesis including acetyl-CoA carboxylase, fatty acid synthase, ATP-citrate lyase and glucose-6-phosphate dehydrogenase decreased as the dietary level of sesamin increased in Exp. 1 and in rats fed the 0.2% sesamin diet they were approximately one-half those in animals fed a sesamin-free diet. In Exp. 2, the 0.2% sesamin diet lowered these parameters to one-half the level for a sesamin-free diet, but no further reduction was seen in animals fed the 0.4% sesamin diet. Dietary sesamin dose-dependently decreased the sterol regulatory element binding protein-1 (SREBP-1) mRNA level, and the value in rats fed a 0.4% sesamin diet was approximately one-half that in those fed a sesamin-free diet. The protein content of the membrane-bound precursor form of SREBP-1 decreased as dietary sesamin increased and was 37% lower in rats fed the 0.4% sesamin diet than in those fed a sesamin-free diet. Dietary sesamin exerted a more marked influence on the protein content of the mature nuclear form of SREBP-1. Diets containing 0.2 and 0.4% sesamin lowered the amount of mature SREBP-1 protein to less than one-fifth of that in the animals fed a sesamin-free diet. It was suggested that the dietary sesamin-dependent decrease in lipogenic enzyme gene expression is due to the suppression of the gene expression of SREBP-1 as well as the proteolysis of the membrane-bound precursor form of this transcriptional factor to generate the mature form.

: Forum Nutr. 2009;61:10-24. Epub 2009 Apr 7. Links
Lipid metabolism and nutrigenomics - impact of sesame lignans on gene expression profiles and fatty acid oxidation in rat liver.Ide T, Nakashima Y, Iida H, Yasumoto S, Katsuta M.
National Food Research Institute, Tsukuba, Japan. [email protected]

The impact of sesamin, episesamin and sesamolin (sesame lignans) on hepatic gene expression profiles was compared with a DNA microarray. Male Sprague-Dawley rats were fed experimental diets containing 0.2% sesamin, episesamin or sesamolin, and a control diet free of lignans for 15 days. Compared to a lignan-free diet, a diet containing sesamin, episesamin and sesamolin caused more than 1.5- and 2-fold changes in the expression of 128 and 40, 526 and 152, and 516 and 140 genes, respectively. The lignans modified the mRNA levels of not only many enzymes involved in hepatic fatty acid oxidation, but also proteins involved in the transportation of fatty acids into hepatocytes and their organelles, and in the regulation of hepatic concentrations of carnitine, CoA and malonyl-CoA. It is apparent that sesame lignans stimulate hepatic fatty acid oxidation by affecting the gene expression of various proteins regulating hepatic fatty acid metabolism. The changes in the gene expression were generally greater with episesamin and sesamolin than with sesamin. In terms of amounts accumulated in serum and the liver, the lignans ranked in the order sesamolin, episesamin and sesamin. The differences in bioavailability among these lignans appear to be important to their divergent physiological activities. We also confirmed that dietary sesame seed affected the expression of genes related to fatty acid oxidation in a manner similar to isolated lignan compounds.