Abstract
Obesity is associated with an increased risk of non-alcoholic fatty liver disease (NAFLD), which is initiated by adipocyte-macrophage crosstalk. Among the possible molecules regulating this crosstalk, we focused on neuropeptide Y (NPY), which is known to be involved in hypothalamic appetite and adipose tissue inflammation and metabolism. In this study, the NPY−/− mice showed a marked decrease in body weight and adiposity, and lower free fatty acid and adipose inflammation without food intake alteration during a high fat diet (HFD). Moreover, NPY deficiency increased the thermogenic genes expression in brown adipose tissue. Notably, NPY-mRNA expression was upregulated in macrophages from the HFD mice compared to that from the mice on a standard diet. The NPY-mRNA expression also positively correlated with the liver mass/body weight ratio. NPY deletion alleviated HFD-induced adipose inflammation and liver steatosis. Hence, our findings point toward a novel intracellular mechanism of NPY in the regulation of adipocyte-macrophage crosstalk and highlight NPY antagonism as a promising target for therapeutic approaches against obesity and NAFLD.
Highlights
Deletion of neuropeptide Y (NPY) in Mouse Protects against High-Fat Diet (HFD)-Induced Obesity
Male NPY+/+ wild type (WT) mice fed an high fat diet (HFD) has grown significantly more com−/− knockout (KO) mice on an compared to the mice on the standard CRF1
We found that mRNA expression of Ucp1 was not increased by NPY deficiency, mRNA expression of other thermogenic genes was partly upregulated in brown adipose tissue (BAT)
Summary
Fat is an indispensable component of the cell membrane and acts as an insulator and energy source in mammals [1]. Excessive fat accumulation may lead to obesity and impaired metabolic homeostasis [2]. Obesity is a growing epidemic and is associated with several metabolic disorders, such as hypertension, hyperglycemia, and dyslipidemia, collectively termed metabolic syndrome [3,4]. The prevalence of obesity in adult as well as children has increased dramatically over the last several decades [5]. The non-alcoholic fatty liver disease (NAFLD), characterized by a progressive fat deposition in the liver, is a consequence of obesity in all ages and may increase the incidence of more serious liver dysfunction, such as non-alcoholic steatohepatitis, fibrosis, and cirrhosis [6]
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