Epigenomic and metabolic responses of hypothalamic POMC neurons to gestational nicotine exposure in adult offspring.

ABSTRACT:

Background

Epidemiological and animal studies have reported that prenatal nicotine exposure (PNE) leads to obesity and type-2 diabetes in offspring. Central leptin-melanocortin signaling via hypothalamic arcuate proopiomelanocortin (POMC) neurons is crucial for the regulation of energy and glucose balance. Furthermore, hypothalamic POMC neurons were recently found to mediate the anorectic effects of nicotine through activation of acetylcholine receptors. Here, we hypothesized that PNE impairs leptin-melanocortinergic regulation of energy balance in first-generation offspring by altering expression of long non-coding RNAs (lncRNAs) putatively regulating development and/or function of hypothalamic POMC neurons.

Methods

C57BL/6J females were exposed ad libitum to nicotine throu

SUBMITTER: Silva JP 

PROVIDER: S-EPMC5015242 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature