Changes in Expression of Follicular Glucose Transporters May Be Involved in Ovarian Function Impairment during

Bin Xu1, Ying Hu2, Ya-Ting Luo1

  • 1Department of Physiology, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Sichuan, Chengdu, China.

Insights

Type 1 diabetes impairs ovarian function by reducing glucose transporter expression in follicles. This leads to decreased glucose uptake, energy deprivation, and abnormal egg maturation and ovulation.

Area of Science:

  • Reproductive biology
  • Endocrinology
  • Metabolic disorders

Background:

  • Diabetes-induced hyperglycemia negatively impacts ovarian function.
  • The precise mechanisms underlying diabetes-related ovarian impairment are not fully understood.
  • Glucose transporters are crucial for cellular glucose uptake and utilization, but their specific roles in ovarian dysfunction during diabetes remain unclear.

Purpose of the Study:

  • To investigate glucose transporter expression in ovarian follicles of patients with type 1 diabetes mellitus.
  • To elucidate the role of glucose transporters in diabetes-induced ovarian function impairment.
  • To analyze the relationship between glucose transporters, adenosine monophosphate-activated protein kinase (AMPK), and ovarian function in a mouse model of type 1 diabetes.

Main Methods:

  • Evaluation of ovarian function in a mouse model of type 1 diabetes mellitus, including estrus cycle, follicular development, and ovulation.
  • Analysis of the expression of glucose transporter subtypes (GLUT2, GLUT3, GLUT4, SGLT1, SGLT2), AMPK, and phosphorylated AMPK (Thr172) in ovarian follicle cells.
  • Comparison of these markers between diabetic and non-diabetic control mice.

Main Results:

  • Diabetic mice exhibited dysregulated estrus cycles and a higher incidence of abnormal ova compared to controls.
  • Expression of multiple glucose transporters was found to be downregulated in diabetic mice relative to phosphorylated AMPK.
  • Increased levels of phosphorylated AMPK were observed in follicular granulosa cells and oocytes of diabetic mice.

Conclusions:

  • Diabetes-induced hyperglycemia reduces ovarian follicle cell capability by downregulating glucose transporter expression.
  • This downregulation leads to diminished glucose uptake and energy deficits within ovarian cells.
  • The observed changes suggest a mechanism for impaired egg maturation and ovulation in diabetic conditions.

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