Palmitoleic acid n-7 in the modulation of glucose metabolism and oxidative stress in human visceral adipose tissue in vitro
Name: NAYARA ARIEL DA SILVA LISBOA
Publication date: 09/04/2026
Examining board:
Name |
Role |
|---|---|
| ANDRESSA BOLSONI LOPES | Presidente |
| LORENA BARROS FURIERI | Examinador Interno |
| MARIA ISABEL CARDOSO ALONSO-VALE | Examinador Externo |
Summary: Introduction: Obesity associated dysfunction of visceral white adipose tissue (vWAT)
is characterized by impaired glucose handling, altered adipokine secretion, and redox
imbalance, contributing to systemic metabolic deterioration. Palmitoleic acid (16:1n-7),
a bioactive monounsaturated fatty acid, has been implicated in the regulation of
glucose and lipid metabolism in rodent and cellular model; however, its effects on
human adipocytes under metabolically compromised conditions remain incompletely
understood. Objective and Methods: Here, we investigated the effects of in vitro
treatment with 16:1n-7 on glucose uptake and metabolism and oxidative stress in
visceral adipocytes derived from women with obesity and prediabetes.16:1n7
increased basal and insulin-stimulated glucose uptake in association with upregulation
of GLUT1 and GLUT4 expression and increased AMPK protein content. In parallel,
16:1n-7 promoted coordinated changes in metabolic gene expression favoring glucose
utilization and glyceroneogenesis rather than de novo lipogenesis. Endocrine function
was also modulated, as 16:1n-7 reduced resistin secretion without impairing
adiponectin levels. Moreover, although lipid peroxidation remained unchanged,
palmitoleic acid reduced protein oxidation and reactive oxygen species production,
together with increased IDH2 and reduced iNOS expression, supporting selective
attenuation of oxidative stress. Conclusion: The 16:1n-7 enhances glucose uptake
through coordinated regulation of GLUT1 and GLUT4 and contributes to improved
metabolic and redox homeostasis in visceral adipocytes derived from human with
obesity and prediabetes. These findings identify 16:1n-7 as a direct modulator of
human adipocyte function under metabolically compromised conditions and support
further investigation of its relevance in metabolic disease.
