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 Lipid Signaling and Obesity Research

Obesity Research
 

The metabolism and storage of lipids in the body is accomplished using a number of different enzymes. 11b -Hydroxysteroid dehydrogenase type 1 and 2 (11b-HSD1 and 2) aid in the conversion of cortisone to cortisol. 11b-Hydroxysteroid dehydrogenase type 1 (11b-HSD1) is expressed in adipose tissue. Over expression of this enzyme along with increased levels of glutacorticoid causes an accumulation and an increase in visceral adipocytes. Increased cortisol levels cause Cushing’s syndrome, which triggers obesity in individuals. Another key enzyme in lipid metabolism is Acyl coenzyme A: diacylglycerol acyltransferase 1 (DGAT1). DGAT1 is involved with the synthesis of triglycerides, which are the main form of excess calorie storage in fat. Both gastric and pancreatic lipases regulate dietary fat digestion. To limit fat digestion, inhibitors such as orlistat have been developed to inhibit these lipases. Fatty acid synthase inhibitors can possibly reduce food intake. Inhibiting any of these metabolic enzymes could be a potential therapeutic approach for obesity treatment.



Palmitoylation and Myristoylation
Product #  Product Name Notes Add to Cart
C2389 Cerulenin from Cephalosporium caerulens Antibiotic; fatty acid synthase inhibitor.
P4509 Palmitoyl-DL-Carnitine chloride Long-chain acylcarnitine and well-known intermediate in mitochondrial fatty acid oxidation. Modifies myocardial levels of high-energy phosphates and free fatty acids in the heart. Increases erythroid colony formation in culture. Reduces surface negative charge of erythrocytes and myocytes.

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