Glucagon-Stimulated Lipolysis of Primary Cultured Broiler Adipocytes

Abstract

A procedure for maintaining broiler adipocytes in culture was established and used to evaluate the effect of selected culture ingredients on glucagon-stimulated lipolysis. Adipocytes were isolated by collagenase and trypsin digestion of abdominal adipose tissue from 40- to 70-day-old broilers. Freshly isolated adipocytes did not exhibit glucagon-stimulated lipolysis. However, after 24 h in culture, lipolysis was stimulated maximally at doses of glucagon from 5 to 100 ng/mL with 50% stimulation occurring at .7 +/- .4 ng/mL. This responsiveness was maintained for an additional 24 h in culture. Inclusion of 2 or 5% chicken serum in the medium reduced (P less than or equal to .05) the responsiveness of the cells to glucagon. A 30% reduction (P less than or equal to .001) in responsiveness occurred when bovine serum albumin was removed from the medium. The results indicate that broiler adipocytes can be maintained in culture and that certain culture ingredients alter the responsiveness of the cells to glucagon.

SSTR2 Mediates the Inhibitory Effect of SST/CST on Lipolysis in Chicken Adipose Tissue

“…In this study, we investigated the effects of glucagon, SST28, CST14, and CYN-154806 (SSTR2 antagonist) on glycerol release in cultured chicken adipose tissues. By detecting the concentration of glycerol in the incubation solution, GCG significantly stimulated the lipolysis of chicken adipose tissue, which was consistent with previous reports [23,24,51]. SST28 and CST14 alone did not affect the release of glycerol in adipose tissue, indicating that SST28 and CST14 did not affect basal lipolysis.…”

“…In isolated chicken adipocytes, Strosser et al have found that SST14 and SST28 inhibit glucagon-stimulated glycerol release [23]. Glucagon is the main lipolytic hormone in domestic chickens and transmits signals through the glucagon receptor (GCGR) [24][25][26][27]. In pancreatectomized or hypophysectomized ducks, somatostatin infusion resulted in a decrease in plasma-free fatty acid, suggesting a direct anti-lipolytic effect of somatostatin on adipose tissue [28].…”

Role of Corticosterone in Lipid Metabolism in Broiler Chick White Adipose Tissue

“…Six 10-day-old chicks were euthanized by decapitation and abdominal WAT was excised. Adipocytes were isolated as described previously (Oscar et al, 1991), and then incubated with Dulbecco's Modified Eagle Medium (DMEM, 1.0 g/L glucose with L-glutamine and sodium pyruvate; 08456-65, Nacalai Tesque, Inc.) containing 25 mM HEPES, 80 µg/ml kanamycin, and 3% bovine serum albumin, supplemented with either 0 (control) or 1,040 μg/mL corticosterone (Sigma-Aldrich Japan K.K., Tokyo, Japan) for 16 h. After removing the culture medium, the cells were washed twice with PBS and used for real-time PCR analysis. The mRNA levels of lipid metabolism-related genes in adipocytes and the NEFA concentration in the medium were analyzed as described in Experiment 1.…”

Fasting and Glucagon Stimulate Gene Expression of Pyruvate Dehydrogenase Kinase 4 in Chickens

“…It seems likely that glucocorticoids stimulate TG hydrolysis in chicken WAT. However, the effect of glucagon on the expression of lipid metabolism-related genes, such as DGAT2, PDK4, and ATGL, in WAT has not been examined, although it is known that glucagon is the major lipolytic hormone in chickens (Goodridge, 1968;Oscar, 1991, Scanes, 2009). There is evidence that fasting significantly elevated plasma glucagon levels in broiler chickens (Dupont et al, 2008;Richards and McMurtry, 2008;Christensen et al, 2013).…”