HEPATIC MITOCHONDRIAL METABOLISM DURING INSULIN RESISTANCE

$10,458P41FY2010RRNIH

Ut Southwestern Medical Center, Dallas TX

Investigators

Linked publications, trials & patents

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Abstract

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. When carbohydrate intake exceeds short-term requirements for energy, it is stored as fat. The liver is the principle organ responsible for the conversion of excess carbohydrate to fat. Ingesting a high carbohydrate diet induces gene transcription of over a dozen enzymes in liver that are involved in glycolysis and fat synthesis. Insulin, secreted by the pancreas in response to carbohydrate promotes lipogenesis by activating lipogenic enzyme expression. The purpose of this project is to use 2H and 13C NMR methods to analyze hepatic production of glucose in a variety of animal models and human subjects.

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