2nd Edition of International Obesity and Metabolism Conference 2026

Abstract

Abstract

Adipocyte dysfunction, characterized by chronic inflammation and impaired lipid metabolism, is a hallmark of obesity. While beige adipocytes are potential therapeutic targets due to their thermogenic capacity, their metabolic resilience under stress remains poorly understood. This study aimed to compare the phenotypic plasticity of 3T3 L1 (white) and D16 (thermogenically primed) adipocytes by investigating their respective responses to lipotoxic stress (TNF alpha and Palmitate) and beta 3 adrenergic activation (CL 316243).

Differentiated 3T3 L1 and D16 adipocytes were treated for 24 hours with either TNF alpha (10 ng/mL) and Palmitate (0.75 mM) or CL 316243 (1 or 10 mM). We assessed mitochondrial activity, lipolysis, lipid accumulation, adipokine secretion, and gene expression.

In 3T3 L1 adipocytes, TNF alpha and Palmitate significantly increased lipolysis and lipid accumulation, alongside the downregulation of lipid metabolic regulators Ppary, Lipe, and Pgcla. Beta 3 adrenergic stimulation in 3T3 L1 cells increased lipolysis and inflammatory markers (IL 6, Mcp 1).

In contrast, D16 adipocytes exhibited minimal lipolytic and transcriptional responses to stress. While lipid accumulation increased, beta 3 adrenergic stimulation paradoxically reduced Ucp 1 expression.

These findings suggest that intrinsic cellular programming dictates how different adipocyte lineages interpret external stimuli. Consequently, while 3T3 L1 adipocytes serve as a robust model for studying metabolic dysfunction and inflammatory responses, D16 adipocytes represent a thermogenically primed, inflammation resilient phenotype, establishing a functional framework for future lineage specific metabolic research.