Abstract
Neuropeptide Y (NPY) is an orexigenic neuropeptide that plays a role in regulating adiposity by promoting energy storage in white adipose tissue and inhibiting brown adipose tissue activation in mammals. This review describes mechanisms underlying NPY’s effects on adipose tissue energy metabolism, with an emphasis on cellular proliferation, adipogenesis, lipid deposition, and lipolysis in white adipose tissue, and brown fat activation and thermogenesis. In general, NPY promotes adipocyte differentiation and lipid accumulation, leading to energy storage in adipose tissue, with effects mediated mainly through NPY receptor sub-types 1 and 2. This review highlights hypothalamus-sympathetic nervous system-adipose tissue innervation and adipose tissue-hypothalamus feedback loops as pathways underlying these effects. Potential sources of NPY that mediate adipose effects include the bloodstream, sympathetic nerve terminals that innervate the adipose tissue, as well as adipose tissue-derived cells. Understanding the role of central vs. peripherally-derived NPY in whole-body energy balance could shed light on mechanisms underlying the pathogenesis of obesity. This information may provide some insight into searching for alternative therapeutic strategies for the treatment of obesity and associated diseases.
Highlights
Obesity is defined as a state of increased adiposity resulting from chronic nutrient excess, where energy intake significantly exceeds energy expenditure [1]
We demonstrated that Neuropeptide Y (NPY), Neuropeptide Y receptor sub-type 1 (NPYR1), Neuropeptide Y receptor sub-type 2 (NPYR2) and NPY receptor sub-type 5 (NPYR5) mRNA were expressed in chicken abdominal fat, albeit at lower quantities than in the hypothalamus, with differential expression between chickens selected for low or high body weight, and highly negative heterosis, suggesting a role for the NPY system in energy balance in chickens [34]
Conditional knockdown of NPYR2 by an adenoviral vector injected into the subcutaneous abdominal fat of mice led to a 50% reduction in stress-induced fat expansion after 2 weeks [30]. These results collectively suggest that those NPY-mediated effects on adipose tissue were occurring mainly through NPYR2 [30]
Summary
Obesity is defined as a state of increased adiposity resulting from chronic nutrient excess, where energy intake significantly exceeds energy expenditure [1]. Knockdown of NPY expression using adeno-associated virus-mediated RNAi in the dorsomedial nucleus (DMN) of rat hypothalamus promoted development of brown adipocytes in inguinal white adipose tissue or transformation from WAT to BAT ( known as brown-in-white, beige or brite cells) characterized by increases in mitochondrial UCP1 and peroxisome proliferator activated receptor-γ coactivator −1 α (PGC1α) expression, when measured at 16 weeks post treatment This led to increased BAT activity and thereby enhanced energy expenditure and cold-induced thermogenesis [68]. Reduced SNS outflow decreases release of NE from sympathetic nerve endings and inhibits the thermogenic function of brown adipose tissue (BAT) by deactivating the cAMP-dependent PKA pathway, which further down-regulates UCP1-associated thermogenesis Taken together, these data indicate that NPY promotes positive energy balance by stimulating adipogenesis and inhibiting lipolysis in WAT.
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