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Novel lean type 2 diabetic rat model using gestational low-protein programming.

Chellakkan S Blesson1, Amy K Schutt1, Meena P Balakrishnan1

  • 1Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX.

American Journal of Obstetrics and Gynecology
|February 14, 2016
PubMed
Summary
This summary is machine-generated.

Gestational low-protein (LP) diet programming in rats creates a lean model of type 2 diabetes (T2D). This model exhibits progressive glucose intolerance and insulin resistance, particularly in females, without causing obesity.

Keywords:
gestational programmingglucose intoleranceinsulin resistancelean diabetestype 2 diabetes

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Area of Science:

  • Endocrinology
  • Metabolic Diseases
  • Developmental Biology

Background:

  • Type 2 diabetes (T2D) in lean individuals is understudied, yet accounts for a significant portion of diabetes cases.
  • The etiology of lean T2D is poorly understood, with early developmental nutrition implicated.
  • Gestational nutritional programming is a potential factor influencing long-term metabolic health.

Purpose of the Study:

  • To establish a novel rodent model for lean type 2 diabetes (T2D).
  • To investigate the effects of gestational low-protein (LP) diet on metabolic health in offspring.
  • To characterize glucose intolerance and insulin resistance in a lean T2D model.

Main Methods:

  • Pregnant rats were fed either a control (20% protein) or an isocaloric low-protein (LP, 6%) diet.
  • Offspring underwent glucose tolerance tests and euglycemic-hyperinsulinemic clamp studies at various ages.
  • Body fat composition was assessed using MRI and direct measurement post-sacrifice.

Main Results:

  • Gestational LP exposure induced glucose intolerance and insulin resistance (IR) in both male and female offspring.
  • Glucose intolerance and IR were more severe and progressed faster in females than males.
  • No significant differences in body fat content or BMI were observed between LP and control groups, confirming a lean phenotype.

Conclusions:

  • Gestational low-protein programming effectively generates a progressively worsening type 2 diabetes model in lean rats.
  • This model is valuable for studying T2D in non-obese individuals.
  • The findings highlight the critical role of maternal nutrition in programming offspring metabolic disease risk.