Breaking the Diabesity Cycle: Unveiling New Research on Obesity and Diabetes

Breaking the Diabesity Cycle: Unveiling New Research on Obesity and Diabetes

Obesity and diabetes are two of the most pressing health challenges facing society today, impacting millions and often occurring hand in hand. As obesity rates have soared to epidemic levels, Type 2 diabetes has followed suit. While researchers have long known of this connection, only recently have they begun to uncover the complex mechanisms linking these conditions.

The Connection Between Obesity and Diabetes

Diabetes comes in two primary forms: Type 1, an autoimmune condition usually diagnosed in childhood, and Type 2, which often develops later in life due to lifestyle factors like diet and physical activity. Closely tied to obesity, Type 2 diabetes now affects millions in the U.S., with many more at risk as pre-diabetic (CDC National Diabetes Statistics Report, 2024). 

Obesity, defined by excess body fat and commonly measured by BMI, impacts over 40% of U.S. adults (CDC Obesity, 2024). The rise in obesity rates has driven a parallel rise in Type 2 diabetes cases, a relationship so intertwined that experts have coined the term “diabesity” (Golay and Ybarra, 2005).

While not all individuals with diabetes are overweight, carrying excess weight significantly raises the risk of diabetes. Obesity contributes to Type 2 diabetes primarily by impacting insulin function; as body fat increases, cells become less responsive to insulin, leading to elevated blood sugar. Research indicates that people with obesity are three to seven times more likely to develop Type 2 diabetes, with severe obesity (BMI over 35) increasing this risk up to 20 times (Rogers and Still, 2009).


Animal Models in Diabetes and Obesity Research

Exciting new research is targeting the mechanisms connecting obesity and diabetes, with therapies aimed at reducing insulin resistance and fat-induced inflammation. Advanced animal models play a vital role in studying these conditions and how obesity affects insulin and blood sugar regulation, enabling scientists to explore potential therapies. 

Biocytogen’s specialized models, designed to replicate key aspects of obesity and diabetes, are driving progress and accelerating the development of effective therapies.


High-Fat Diet-Induced Obese (DIO) Mouse Model

The High-Fat DIO Mouse Model is a powerful tool for studying obesity-related metabolic disorders, including Type 2 diabetes. By consuming a diet composed of 60% kcal from fat, these mice develop key pathophysiological changes that closely resemble human conditions.


Characterization of High-Fat Diet-Induced Obese (DIO) Mouse Model. (A-B) Glucose tolerance after HFD induction. (B) Area under the curve for (A). (C-F) Blood biochemical analysis after HFD induction. Mean ± SEM, n=10 mice per group.


Spontaneous Diabetes Model (B-ob/ob Mice, leptin deficient mice)

The B-ob/ob mouse model is a specialized tool for studying obesity and high blood sugar (hyperglycemia). These mice lack exons 2 and 3 of the leptin gene, which is essential for maintaining energy balance and body weight. 

Anti-obesity and Hypoglycemic Effects of Dulaglutide in B-ob/ob Mice. (A-B) Body weight and blood glucose changes in B-ob/ob mice from 4 to 21 weeks of age. (C-F) Nine-week-old B-ob/ob mice received 1 mg/kg dulaglutide (in-house) twice weekly for 4 weeks. Body weight and blood glucose were recorded at the indicated times. Glucose tolerance tests were performed the day after the last dose (n = 8 mice per group).


Drug-targeted humanized GLP1R mice (B-hGLP1R mice)

GLP1R signaling enhances glucose-dependent insulin secretion, crucial for diabetes management. Biocytogen’s humanized GLP1R mouse model, with the mouse gene replaced by the human version, offers a powerful tool for in vivo evaluation of GLP1R-targeting drugs.

Efficacy Study of Semaglutide in HFD-Induced B-hGLP1R Mice. (A) Body weight change after HFD induction. (B-D) Body weight change following semaglutide treatment (an antidiabetic and anti-obesity medication for type 2 diabetes and long-term weight management). (E-F) Effect of semaglutide on food intake. (G) Blood glucose change after semaglutide treatment. (H) Glucose tolerance following treatment. (I) Area under the curve for (H). (J) Plasma insulin level. Mean ± SEM. N = 8–10 mice per group.


STZ-Induced Diabetes ModelThe STZ-induced diabetes model uses streptozotocin (STZ) to selectively destroy pancreatic β-cells, effectively mimicking type 1 diabetes. This model is essential for studying the disease and testing therapies targeting insulin production and blood glucose control.

Hypoglycemic Effect of GCGR Antibody in STZ-Induced B-hGCGR Mice. (A-B) Body weight and blood glucose changes in 6-week-old B-hGCGR mice after STZ (50 mg/kg) induction. (C-D) Three weeks after STZ induction, GCGR antibody (10 mg/kg, produced in-house) was administered once per week. Non-fasting blood glucose (C) and fasting blood glucose (D) were measured. Mean ± SEM.


Ready to make strides in diabetes and obesity research? Contact us to explore how our advanced animal models can help drive your next breakthrough!

 

Reference

CDC, National Diabetes Statistics Report, 2024

CDC, Obesity, 2024

Rogers, Joanne Z., and Christopher D. Still. “Obesity and type 2 diabetes.” Obesity Action Coalition (OAC) (2009).

Golay, Alain, and Juan Ybarra. “Link between obesity and type 2 diabetes.” Best practice & research Clinical endocrinology & metabolism 19.4 (2005): 649-663.

Maribao, V. (2023). Here’s How Obesity and Diabetes Are Connected. 



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