Gastric bypass up-regulates insulin signaling pathway

Nutrition. 2011 Jan;27(1):73-80. doi: 10.1016/j.nut.2010.08.005.

Abstract

Objective: In the severely obese, Roux-en-Y gastric bypass (RYGB) reverses diabetes before body weight loss occurs. We determined changes in protein expression of insulin receptor (IR), its substrates (IRS1 and IRS2), and their phosphorylated state (p-IR and p-IRS1/2) in skeletal muscle (SM), liver and adipose tissue (AT), and GLUT4 in SM and AT, 14 and 28 d after RYGB to gaining insight into the time-related dynamics of insulin transduction pathway that may contribute to diabetes resolution.

Background: RYGB induces a rapid weight loss followed by a slower weight loss period, leading to reversal of diabetes. We hypothesize that diabetes reversal is due to RYGB-induced up-regulation of insulin signaling pathway.

Methods: Diet-induced obese rats had RYGB or sham-operation (obese-controls). Daily food intake, body weight, glucose, insulin, and adiponectin were measured. IR, IRS1, IRS2, p-IR, and p-IRS1/2 were measured in SM, liver, and AT and GLUT4 in SM and AT, 14 and 28 d after RYGB, respectively, reflecting the rapid and slower weight loss periods after RYGB.

Results: On day 14, in RYGB rats versus obese-controls, food intake, body weight, and fat mass decreased. Rats became normo-glycemic and had low insulin levels and elevated glucose:insulin ratio and decreased adiponectin concentrations. This persisted to day 28, except that adiponectin rose. No change in IR occurred on day 14, in RYGB rats versus obese-controls. By day 28 RYGB rats had a higher IR expression in SM and liver, but no changes in AT. RYGB induced a time-related increase in p-IR in liver and in pIRS1/2 in SM and liver. An increase in GLUT4 occurred by day 28 in SM and AT.

Conclusions: Improvement in diabetes occurred after RYGB due to up-regulation in key insulin pathway proteins at several levels, predominantly in SM and liver in association with ongoing caloric restriction, body weight, and fat mass loss.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adiponectin / blood
  • Adipose Tissue / metabolism
  • Animals
  • Blood Glucose / metabolism
  • Body Mass Index
  • Diabetes Mellitus / metabolism*
  • Diabetes Mellitus / therapy
  • Disease Models, Animal
  • Energy Intake
  • Gastric Bypass*
  • Glucose Transporter Type 4 / blood
  • Insulin / blood*
  • Insulin Receptor Substrate Proteins / metabolism*
  • Liver / metabolism
  • Male
  • Muscle, Skeletal / metabolism
  • Obesity / metabolism
  • Obesity / surgery*
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, Insulin / metabolism*
  • Signal Transduction*
  • Up-Regulation
  • Weight Loss

Substances

  • Adiponectin
  • Blood Glucose
  • Glucose Transporter Type 4
  • Insulin
  • Insulin Receptor Substrate Proteins
  • Receptor, Insulin