Altered lipid partitioning and glucocorticoid availability in CBG-deficient male mice with diet-induced obesity.

Objective: To evaluate how deficiency in corticosteroid-binding globulin (CBG), the specific carrier of glucocorticoids, affects glucocorticoid availability and adipose tissue in obesity.

Methods: C57BL/6 (WT) and CBG-deficient (KO) male mice were fed during 12 weeks with standard or hyperlipidic diet (HL). Glucocorticoid availability and metabolic parameters were assessed.

Oleoyl-estrone is a precursor of an estrone-derived ponderostat signal.

Oleoyl-estrone (OE) is a powerful anti-obesity compound that decreases food intake, decreases insulin resistance and circulating cholesterol. OE stimulates a severe loss of body fat by decreasing adipose tissue lipid synthesis and maintaining lipolysis. Therefore, the body economy loses lipid energy because energy expenditure is maintained.

Comparative effects of oleoyl-estrone and a specific beta3-adrenergic agonist (CL316, 243) on the expression of genes involved in energy metabolism of rat white adipose tissue.

Background: The combination of oleoyl-estrone (OE) and a selective beta3-adrenergic agonist (B3A; CL316,243) treatment in rats results in a profound and rapid wasting of body reserves (lipid).

Methods: In the present study we investigated the effect of OE (oral gavage) and/or B3A (subcutaneous constant infusion) administration for 10 days to overweight male rats, compared with controls, on three distinct white adipose tissue (WAT) sites: subcutaneous inguinal, retroperitoneal and epididymal. Tissue weight, DNA (and, from these values cellularity), cAMP content and the expression of several key energy handling metabolism and control genes were analyzed and computed in relation to the whole site mass.

Short-term oral oleoyl-estrone decreases the expression of ghrelin in the rat stomach.

Oleoyl-estrone (OE) mobilizes body fat and decreases food intake. The precise mechanism of its modulation of appetite is unknown. Since the effects of OE on food intake appear early, here we studied the effect of OE on the expression of gut peptides that affect short-term ingestive behavior: ghrelin, leptin, CCK, PYY, and GLP-1.

Effects of combined oleoyl-estrone and rimonabant on overweight rats.

Oleoyl-estrone (OE) decreases appetite, maintains energy expediture, induces lipolysis (sparing protein), and decreases cholesterolemia and insulin resistance. Rimonabant (SR141716) is a cannabinoid-receptor inhibitor that decreases appetite and mobilizes fat. We studied whether their combination improves their slimming effects.

Combined effects of oleoyl-estrone and a beta3-adrenergic agonist (CL316,243) on lipid stores of diet-induced overweight male Wistar rats.

Oleoyl-estrone (OE) decreases appetite, induces adipose tissue wasting and resets the ponderostat setting, sparing glucose and protein. The beta3-adrenergic agonists increase energy expenditure and lipolysis. We studied the combination of both treatments to enhance fat mobilization.

Effects of oleoyl-estrone with dexfenfluramine, sibutramine or phentermine on overweight rats.

We studied the combination of oleoyl-estrone with either dexfenfluramine, sibutramine or phentermine in overweight male rats treated for 10 days in order to determine whether they shared a mechanism of action. Oleoyl-estrone, dexfenfluramine and sibutramine decreased body weight and energy (essentially lipids); losses were higher when combined with oleoyl-estrone. Glycemia was maintained except under phentermine; oleoyl-estrone induced decreases in triacylglycerols, cholesterol, insulin and HOMA (homeostasis model assessment).