Genistein diet improves body weight, serum glucose and triglyceride levels in both male and female ob/ob mice

Abstract

Purpose

Diabetic obesity in the leptin-deficient ob/ob mouse is associated with weight gain, and hyperglycemia, along with hyperinsulinemia. We have previously examined the effects of genistein (a naturally occurring isoflavone found in soy) on metabolic disturbances in the ob/ob mouse and demonstrated beneficial effects of genistein (600 mg genistein/kg diet, for 4-weeks) on T₃ production and corticosterone status. The goal of this study was to examine whether dietary genistein could prevent, or at least lessen, the typical phenotype in this murine model of diabetic-obesity, and to assess potential sex-differences.

Patients and methods

The ob/ob mice (male and female) aged 4–5 weeks were randomly assigned to one of two diets for a period of 4-weeks: standard rodent diet, or genistein-containing diet (600 mg genistein/kg diet). Comparisons were made to a lean control group.

Results

Genistein diet significantly reduced body weight by 12% in females and 9% in males. Genistein significantly lowered serum glucose levels by 18% in females and 43% in males, yet had no effect on serum insulin. Genistein diet significantly lowered serum triglyceride levels in both ob/ob male and female mice returning them to lean levels. In females only, genistein significantly reduced serum pancreatic polypeptide levels by 56% and increased serum GIP levels 2.3-fold. Genistein had sex-dependent effects on hepatic steatosis: in females, genistein further increased the % fat area and the fat droplet diameter 2.6-fold, along with additionally increasing hepatic TBARS.

Conclusion

The results from this study indicate interesting beneficial effects of genistein diet for both male and female ob/ob mice.

Keywords:

• genistein
• ob/ob
• diabetes
• phenotype

Acknowledgments

Schuyler Rockwood was supported through the Department of Biomedical Sciences, College of Health Sciences and the MWU Summer Research Fellowship. This work was supported by Midwestern University Intramural funds (to LA) and Diabetes Action and Research Education Foundation (to LA). We thank Mr. Tatum Banayat for helpful technical assistance.

Disclosure

The authors report no conflicts of interest in this work.