School of Podiatric Medicine - Student Research

Document Type

Poster

Publication Date

7-2026

Abstract

Introduction/Purpose: Obesity has become an epidemic with over six million adult individuals affected by this metabolic condition, and it is associated with over 40% of deaths worldwide. Diabetic kidney disease (DKD) is a major cause of kidney disease globally and it is a major cause of mortalities associated with diabetes. In DKD, impaired glucose regulation results in hyperglycemia-induced metabolic dysfunction that culminate in abnormal energy utilization and mitochondrial dysfunction and play critical role in the pathogenesis of DKD. Incidentally, mitochondrial functions and dynamics are impaired in liver insufficiencies of multiple origins. Prevention of triglyceride and lipotoxic accumulations by hepatic mitochondria is impaired in obesity and predispose to steatohepatitis. Need arises to better understand the interaction and potentiation of diabetes/obesity with nephropathy and hepatic insufficiency. Objective is to determine whether obesity dysregulates mitochondria bioenergetics in renal and hepatic systems.

Methods: Fifteen male C57BL/6J mice (8 weeks old) were fed a high-fat diet (HFD), low-fat diet (LFD), or regular diet (RD, control) for 12 weeks (n = 5/group) (AUP/IACUC: 22-33). Mean body weight (MBW), body size (BS), blood glucose level (BGL) and intraperitoneal glucose tolerance testing (IPGTT) were performed. Liver and kidney tissues were collected for further mitochondrial bioenergetic studies.

Results: Data showed statistical (p < 0.05) significant difference in MDW (g), BS, and BGL/ IPGTT (mg/dL), between LFD-fed, RD and HFD-diet mice.

Conclusion: HFD increased the MBW, BS, and BGL in the mice, consistent with obesity and diabetes-like metabolic dysfunction.

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