Visceral fat and beta cell function in non-diabetic humans

Area of Science:

• Metabolic health and endocrinology
• Obesity research
• Human physiology

Background:

• Visceral adipose tissue (VAT) accumulation is associated with insulin resistance.
• The effect of visceral obesity on pancreatic beta cell function is not fully understood.

Purpose of the Study:

• To investigate the relationship between visceral obesity and beta cell function in non-diabetic adults.
• To determine if excess visceral fat impacts insulin secretion and beta cell dynamics.

Main Methods:

• Magnetic resonance imaging (MRI) to quantify visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT).
• C-peptide deconvolution and physiological modeling of oral glucose tolerance test (OGTT) data to assess insulin secretion and beta cell function.
• Multivariate analysis controlling for sex, age, BMI, and SAT.

Main Results:

• Excess VAT was associated with a phenotype of higher glucose, blood pressure, heart rate, and transaminases.
• Visceral obesity correlated with insulin resistance and hyperinsulinemia, but insulin secretion appropriately compensated for resistance.
• No independent association was found between excess VAT and parameters of beta cell function (glucose sensitivity, rate sensitivity, potentiation).

Conclusions:

• Preferential visceral fat deposition is part of an insulin-resistant phenotype in non-diabetic adults.
• The pancreatic beta cell response adequately compensates for insulin resistance caused by visceral obesity.
• Beta cell function dynamics remain largely preserved despite visceral adiposity.