Publications by authors named "Kendra E Miller"
Article Synopsis
- Hepatic lipid buildup in obesity leads to increased hyperinsulinemia and insulin resistance, affecting liver function.
- Hepatocyte depolarization reduces vagal nerve firing and heightens GABA release, contributing to hyperinsulinemia.
- Altering hepatic GABA release can improve insulin sensitivity and mitigate glucoregulatory issues in obesity, with implications for type 2 diabetes risk.
Hepatic lipid accumulation is a hallmark of type II diabetes (T2D) associated with hyperinsulinemia, insulin resistance, and hyperphagia. Hepatic synthesis of GABA, catalyzed by GABA-transaminase (GABA-T), is upregulated in obese mice. To assess the role of hepatic GABA production in obesity-induced metabolic and energy dysregulation, we treated mice with two pharmacologic GABA-T inhibitors and knocked down hepatic GABA-T expression using an antisense oligonucleotide.
View Article and Find Full Text PDFSignaling through GPR109a, the putative receptor for the endogenous ligand β-OH butyrate, inhibits adipose tissue lipolysis. Niacin, an anti-atherosclerotic drug that can induce insulin resistance, activates GPR109a at nM concentrations. GPR109a is not essential for niacin to improve serum lipid profiles.
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