Glucose Transporter Regulation in Obesity and Diabetes

NIH RePORTER · NIH · R56 · $172,900 · view on reporter.nih.gov ↗

Abstract

Enter the text here that is the new abstract information for your application. This section must be no longer than 30 lines of text. Bridge Funding for DK43051– PI: Barbara B. Kahn, MD Long-term Overall Goal: To determine the mechanisms by which reduction of ChREBP in adipocytes causes systemic insulin resistance and impaired glucose transport in adipocytes. Background: Carbohydrate Response Element Binding Protein (ChREBP) is the major transcription factor regulating de novo lipogenesis (DNL, fatty acid synthesis from glucose) in adipocytes. We showed that adipose-selective ChREBP KO (AdChREBP KO) causes systemic insulin resistance and impairs insulin-stimulated glucose transport in adipocytes. In humans, expression of ChREBP and genes regulating DNL in adipose tissue correlate highly with insulin sensitivity measured by clamp. Specific Aims for One Year: Specific Aim 1: To maintain lab staff Specific Aim 2: To maintain mouse lines Specific Aim 3: To generate additional preliminary data

Key facts

NIH application ID
10553357
Project number
2R56DK043051-29
Recipient
BETH ISRAEL DEACONESS MEDICAL CENTER
Principal Investigator
BARBARA B. KAHN
Activity code
R56
Funding institute
NIH
Fiscal year
2022
Award amount
$172,900
Award type
2
Project period
1992-02-01 → 2023-03-31