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Development and Validation of a Methodology for Establishing Obese Rat Models with Typical Fatty Pancreas

Development and Validation of a Methodology for Establishing Obese Rat Models with Typical Fatty Pancreas

Published on: November 11, 2025

[Abdominal obesity and diabetes].

Enzo Bonora¹, Corinna Brangani, Isabella Pichiri

¹Sezione di Endocrinologia e Malattie del Metabolismo, Dipartimento di Scienze Biomediche e Chirurgiche, Università degli Studi, Verona. enzo.bonora@univr.it

Giornale Italiano Di Cardiologia (2006)

|September 9, 2008

Summary

Visceral obesity, characterized by excess abdominal fat, contributes to metabolic and cardiovascular diseases. Molecules released by visceral fat negatively impact insulin sensitivity and pancreatic beta-cell function, leading to glucose homeostasis abnormalities.

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Area of Science:

Endocrinology
Metabolic Syndrome
Obesity Research

Background:

Different obesity phenotypes have been recognized for decades.
The link between abdominal (visceral) obesity and metabolic/cardiovascular diseases is a recent focus.
The association between abdominal obesity and diabetes is well-established, primarily due to reduced insulin sensitivity.

Purpose of the Study:

To explore the detrimental role of visceral adipocytes and their secreted molecules on beta-cell function.
To investigate how visceral fat accumulation impacts glucose homeostasis.
To elucidate the mechanisms linking visceral obesity to metabolic dysfunction.

Main Methods:

Review of recent studies on visceral adipocyte function and secreted molecules.
Analysis of the impact of free fatty acids and adipokines (e.g., TNF-α, IL-6, adiponectin, leptin, resistin) on beta-cells.
Examination of lipid accumulation (triglycerides, ceramide) in metabolic organs.

Main Results:

Visceral adipocytes release molecules that impair beta-cell function.
Free fatty acids and specific adipokines contribute to beta-cell dysfunction.
Excess visceral fat leads to lipid deposition in the liver, muscle, and islets, exacerbating insulin resistance and beta-cell dysfunction.

Conclusions:

Visceral obesity is a significant risk factor for metabolic and cardiovascular diseases.
Molecules secreted by visceral fat, alongside lipid accumulation, disrupt glucose metabolism.
Understanding these mechanisms is crucial for managing diabetes and related conditions associated with obesity.