An extra virgin olive oil diet impairs glycemic control, but mitigates high-fat diet-induced inflammation compared to coconut oil in mice.

Authors

Lena Keller, Angela J T Bosch, Andy J Y Low, Laura Steiger, Stephan Wueest, Daniel Konrad, Daniel T Meier, Pascale Vonaesch, Claudia Cavelti-Weder

Published in

Frontiers in nutrition. Volume 13. Pages 1776312. Epub Apr 28, 2026.

Abstract

Extra virgin olive oil is widely regarded as a metabolically beneficial dietary component due to its anti-inflammatory and antioxidant properties, but its effects on glucose homeostasis remain inconclusive. The aim of this study was to evaluate the impact of an extra virgin olive oil-based high-fat diet (E-HFD) compared to a macronutrient-matched coconut oil-based HFD (C-HFD) on glucose homeostasis and investigate potential underlying mechanisms, including inflammation, gut microbiota, and metabolic partitioning.
Male C57BL/6N mice (5-7 weeks old) were fed E-HFD, C-HFD, or standard chow for up to 5 months. Glucose, insulin, and pyruvate tolerance tests and glucose-stimulated insulin secretion were performed. Immune cells in the perigonadal adipose tissue, colon, and liver were analyzed by flow cytometry. Metabolic partitioning was assessed by analyses of substrate utilization and lipid metabolism.
E-HFD-fed mice developed glucose intolerance within 1 week, accompanied by a blunted compensatory insulin response compared to C-HFD, which further deteriorated over time. While C-HFD led to increased adipose tissue and colonic inflammation compared to chow, E-HFD showed only mild or no inflammatory changes. Systemic inflammation and cecal microbiota composition were comparable between the HFD groups. Notably, we found increased hepatic lipid accumulation, upregulation of de novo lipogenesis genes, glycogen storage, and increased adipose tissue mass in E-HFD, but not in C-HFD mice, compared to chow after 1 week, indicative of preferential fatty acid storage. In contrast, C-HFD was characterized by increased circulating non-esterified fatty acids and beta-hydroxybutyrate levels compared to E-HFD mice, indicating enhanced fatty acid utilization.
E-HFD induced pronounced glucose intolerance and a blunted compensatory insulin response, while causing less tissue inflammation than C-HFD compared to standard chow. Neither inflammation nor gut microbiota composition accounted for the observed metabolic impairment. Instead, the altered glucose homeostasis was associated with fatty acid storage and enhanced hepatic lipid accumulation. These findings point toward altered metabolic partitioning and suggest the involvement of a liver-pancreas axis in diet-dependent regulation of glucose homeostasis.

PMID:
42131239
Bibliographic data and abstract were imported from PubMed on 12 Sep 2026.

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