Neurosecretory Protein GL Induces Fat Accumulation in Chicks

Adipogenesis is the process by which precursor stem cells differentiate into lipid laden adipocytes. Adipogenesis is regulated by a complex and highly orchestrated gene expression program. In mammalian cells, the peroxisome proliferator-activated receptor γ (PPARγ), and the CCAAT/enhancer binding proteins (C/EBPs) such as C/EBPα, β and δ are considered the key early regulators of adipogenesis, while fatty acid binding protein 4 (FABP4), adiponectin, and fatty acid synthase (FAS) are responsible for the formation of mature adipocytes. Excess accumulation of lipids in the adipose tissue leads to obesity, which is associated with cardiovascular diseases, type II diabetes and other pathologies. Thus, investigating adipose tissue development and the underlying molecular mechanisms is vital to develop therapeutic agents capable of curbing the increasing incidence of obesity and related pathologies. In this review, we address the process of adipogenic differentiation, key transcription factors and proteins involved, adipogenic regulators and potential anti-adipogenic bioactive molecules.

White adipose tissue (WAT) dysfunction plays a key role in the pathogenesis of type 2 diabetes (DM2). Unrestrained WAT lipolysis results in increased fatty acid release, leading to insulin resistance and lipotoxicity, while impaired de novo lipogenesis in WAT decreases the synthesis of insulin-sensitizing fatty acid species like palmitoleate. Here, we show that insulin infused into the mediobasal hypothalamus (MBH) of Sprague-Dawley rats increases WAT lipogenic protein expression, inactivates hormone-sensitive lipase (Hsl), and suppresses lipolysis. Conversely, mice that lack the neuronal insulin receptor exhibit unrestrained lipolysis and decreased de novo lipogenesis in WAT. Thus, brain and, in particular, hypothalamic insulin action play a pivotal role in WAT functionality. Copyright © 2011 Elsevier Inc. All rights reserved.

Because de novo fatty acid synthesis in birds takes place mainly in the liver, adipose tissue growth and subsequent fattening depend on the availability of plasma triglycerides, which are transported as components of lipoproteins. In growing birds, VLDL is the major transporter of triglycerides, and attempts to reduce excessive fatness in poultry have involved the control of VLDL metabolism. Lean and fat lines of chickens have been selected on the basis of either their abdominal fat content or plasma VLDL concentration. In both cases, hepatic lipogenesis or LPL activity in adipose tissue did not differ between lean and fat lines, and therefore they did not appear to be limiting factors of susceptibility to fattening. In contrast, hepatic secretion and plasma concentration of VLDL were always higher in fat chickens than in lean chickens. Thus, current methods of selection of broilers against excessive fatness are based on this direct relationship between plasma VLDL and adiposity. When hepatic lipogenesis exceeds the capacity of VLDL secretion, triglycerides accumulate in the liver, causing steatosis. Although fatty liver is associated with reduced egg production and increased mortality in laying hens, hepatic steatosis in overfed ducks and geese is of positive economic value, serving as the basis for "foie-gras" production. The balance between synthesis and secretion of VLDL is therefore the key point that regulates hepatic and extrahepatic fattening in poultry.