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实验室

10:00-12:00, Wednesday, April 4, 2018


Speaker1: Jay D. Horton, MD

Dr. Robert C. and Veronica Atkins Chair in Obesity and Diabetes,

Scott Grundy’s Director Chair,

Professor of Internal Medicine and Molecular Genetics,

Director of the Center for Human Nutrition,

UT Southwestern Medical Center

Topic:     Targeting Lipogenesis for the Treatment of NAFLD

Host:     Minmin Luo, Ph.D.

Abstract

Obesity and insulin resistance are strongly associated with the development of nonalcoholic fatty liver disease (NAFLD). The excess triglycerides that accumulate in hepatocytes is derived from multiple sources, one of which is de novo lipogenesis. Fatty acid synthesis in liver is regulated by SREBP-1c, ChREBP, and LXR. The first committed enzyme in fatty acid synthesis, acetyl-CoA carboxylase (ACC), is also regulated by phosphorylation/dephosphorylation, and protein polymerization. Previously, we showed that MIG12, a 22 kDa cytosolic protein, binds to ACC and lowers the threshold for citrate-induced ACC activation. All of these factors contribute to the development of hepatic steatosis. Here, we further explore the interrelated molecular and physiological functions of these lipogenic regulators in the development of NAFLD and investigate the feasibility of each as therapeutic targets for the treatment of NAFLD.

Speaker2: Joel K. Elmquist, DVM, Ph.D.

Division of Hypothalamic Research

Departments of Internal Medicine and Pharmacology

University of Texas Southwestern Medical Center

Topic: Leptin Action on POMC Neurons:Why do Leptin Levels Fall with Fasting?

Host:     Minmin Luo, Ph.D.

Abstract

The brain plays a critical role in regulating food intake, body weight and blood glucose levels.  Dysfunction of this regulation results in obesity and diabetes. Key signals act on collection of neurons within the hypothalamus to regulate food intake and body weight and glucose homeostasis. In addition, similar pathways regulate food intake and glucose homeostasis during periods of fasting. However, the inherent complexity of these circuits has made it extremely difficult to identify the key neurons that regulate these processes.  Over the past several years the ability to manipulate gene expression in a neuron-specific fashion has become feasible.  We will describe some our recent findings using mouse models that allow neuron-specific manipulation of genes regulating energy balance and glucose homeostasis. We will explore the role of these circuits during periods of food availability and following other metabolic challenges such as fasting.  We hope to provide insights into the mechanisms through which the brain controls food intake, body weight and blood glucose levels.