Increased lipolysis in Vgf knockout mice

The sympathetic nervous system is an important regulator of glucose and fat metabolism, and its dysfunction can predispose to obesity and type 2 diabetes mellitus. Targeted deletion of VGF, a neuronal and endocrine secreted protein and neuropeptide precursor, produces a lean, hypermetabolic mouse that is resistant to diet-, lesion-, and genetically- induced obesity and diabetes. However, the underlying mechanisms for this are yet to be elucidated. Fargali et al. hypothesised that increased sympathetic nervous system activity in Vgf - /Vgf - knockout mice is responsible for increased energy expenditure and decreased fat storage. They examined WAT to determine the effect that targeted germline ablation of VGF has on fat pad weight and WAT lipolysis and lipogenesis. They found that Vgf knockout mice have reduced body weight, decreased gonadal fat pad weight, and alterations in a number of key lipolytic proteins compared with wild-type mice. Their data suggest that the VGF precursor or selected VGF-derived peptides dampen sympathetic outflow pathway activity to WAT to regulate fat storage and lipolysis. Fargali et al. (2012) Journal of Endocrinology 215 313-322.

Read the full article at: DOI: 10.1530/JOE-12-0172