Regulation of forkhead box O transcription factor by insulin signaling pathway controls the reproductive diapause of the lady beetle, Coccinella septempunctata.

In biological control programs, knowledge about diapause regulation in natural enemy insects provides important insight for improving long-term storage, transportation, and field adoption of these biological control agents. As a natural predator of agricultural pests, the lady beetle Coccinella septempunctata has been commercially mass-cultured and widely employed in pest management. In some insects, insulin signaling, in conjunction with the downstream transcription factor Forkhead box O (FoxO), are master regulators of multiple physiological processes involved in diapause, but it is unclear whether insulin signaling and FoxO affect the diapause of C. septempunctata. In this study, we use a combination of approaches to demonstrate that insulin signaling and FoxO mediate the diapause response in C. septempunctata. In diapausing beetles, application of exogenous insulin and knocking down expression of CsFoxo with RNA interference (RNAi) both rescued beetles from developmental arrest. In non-diapausing beetles, knocking down expression of the insulin receptor (CsInR) with RNA interference (RNAi) arrested ovarian development and decreased juvenile hormone (JH) content to levels comparable to the diapause state. Taken together, these results suggest that a shutdown of insulin signaling prompts the activation of the downstream FoxO gene, leading to the diapause phenotype.

ChREBP and LXRα mediate synergistically lipogenesis induced by glucose in porcine adipocytes.

Glucose is a substrate for fatty acid synthesis, and induces lipogenesis and expressions of lipogenic genes. It was proposed that transcriptional factor ChREBP, LXRα and SREBP-1c are key mediators in lipogenesis induced by glucose, however the underlying mechanism remains unclear in porcine adipocytes. In this study, glucose stimulated lipogenesis and expressions of ChREBP, LXRα, SREBP-1c and lipogenic genes FAS and ACC1 in primary porcine adipocytes. When ChREBP expression was knocked down by RNAi, lipogenesis and FAS and ACC1 expressions decreased significantly, and lipogenesis induced by glucose decreased by 75.6%, whereas neither the basal expressions under glucose-free nor glucose induced expressions of LXRα and SREBP-1c were evidently affected, suggesting that ChREBP was a main mediator of lipogenesis stimulated by glucose. Glucose promoted LXRα gene expression, and activation of LXRα by T0901317 increased SREBP-1c expression and enhanced the stimulation of glucose on lipogenesis, but this stimulatory effect of LXRα depended on glucose. Activated LXRα stimulated lipogenesis and ChREBP mRNA expression, which was much lower than that elevated by glucose, and was markedly lower in ChREBP-silencing than in unperturbed adipocytes. SREBP-1c activation blocked by fatostatin markedly decreased lipogenesis and expressions of FAS and ACC1 induced by glucose. Lipogenesis and lipogenic gene expression stimulated by LXRα activation were attenuated by fatostatin, however there was still a slightly increase in ChREBP-silencing adipocytes. These dates suggested that LXRα could directly or through SREBP-1c mediate the lipogenesis induced by glucose. Together, glucose induced lipogenesis and lipogenic gene expressions directly through ChREBP, and directly through LXRα or via SREBP-1c.

Comparison of the adipogenesis in intramuscular and subcutaneous adipocytes from Bamei and Landrace pigs.

Fat deposition is a complex process involving proliferation, differentiation, and lipogenesis of adipocytes. Bamei and Landrace are considered to represent fat- and lean-type pig breeds. Subcutaneous (SC) and intramuscular (IM) pre-adipocytes were cultured to compare the proliferation and lipogenesis in these breeds. The differentiated adipocytes were exposed to glucose or insulin to evaluate their effects on lipogenesis and lipogenic gene expression. Pre-adipocytes proliferated dramatically faster in SC vs. IM cells, and in Bamei vs. Landrace breeds. Lipogenesis and lipogenic gene expression had a greater increase in Bamei than in Landrace, and in SC vs. IM in the process of differentiation. Glucose markedly promoted lipogenesis and lipogenic gene expression in differentiated adipocytes. The stimulation of high-glucose levels on lipogenesis and ChREBP and lipogenic gene expression was higher in SC than IM adipocytes, and in Bamei vs. Landrace. Insulin largely increased SREBP-1c expression, however it modestly stimulated lipogenesis and lipogenic gene expression, and there was no difference between cell populationsor between breeds. These data demonstrated that regional and varietal differences obviously existed in the development of porcine adipocytes. The proliferation and differentiation capacity of pre-adipocytes, and the adipocyte lipogenesis stimulated by glucose, are stronger in Bamei than Landrace, and in SC vs. IM adipocytes independent of breed.