Effects of β-carotene on glucose metabolism dysfunction in human subjects and type 2 diabetic rats

Preprint | 
10.55415/deep-2022-0016
This is not the most recent version. There is anewer versionof this content available.
Jianjun Wu
Department of Cardiology The Second Affiliated Hospital of Harbin Medical University,Key Laboratory of Myocardial Ischemia Minis
Department of Cardiology The Second Affiliated Hospital of Harbin Medical University,Key Laboratory of Myocardial Ischemia Minis
Yinan Zhou
Department of Digestive internal medicine The First Affiliated Hospital of Harbin Medical University
Department of Digestive internal medicine The First Affiliated Hospital of Harbin Medical University
Fan Yang*
Department of Cardiology The Second Affiliated Hospital of Harbin Medical University,Key Laboratory of Myocardial Ischemia Minis
Department of Cardiology The Second Affiliated Hospital of Harbin Medical University,Key Laboratory of Myocardial Ischemia Minis
Dawei Yang*
Department of Orthopedics The Fourth Affiliated Hospital of Harbin Medical University
Department of Orthopedics The Fourth Affiliated Hospital of Harbin Medical University

# contributed equally to this work, * Corresponding author


Abstract

Background:
Recent epidemiological studies have shown a link between antioxidant carotenoids and type 2 diabetes, but a comprehensive longitudinal study of this link has not yet been conducted.
Methods:
We included participants who had biological measurements for both serum cis-β-carotene and fasting glucose from NHANES (2001–2006). We divided participants into quartiles by the serum cis-β-carotene levels and supported this associations with glucose metabolism using multivariable regression models adjusted for confounding factors. The mechanism of β-carotene levels in regulating plasma glucose levels were further investigated in vivo and in vitro.
Results:
We found that the higher cis-β-carotene (Q4) had a higher LDL-C level but with a lower TG. However, T2DM rats with β-carotene treatment showed decreased total triglycerides and LDL-cholesterol levels (LDL-c). β-carotene showed better cardiac function in DM+ group compared with diabetes groups (P<0.05). Our results also revealed that β-carotene to be an important protective factor of improving cardiac and mitochondrial function with diabetes exposure. At non-cytotoxic doses, β-carotene significantly increased glucose uptake in insulin-resistant cells. This potential effect is mediated by inducing the expression of GLUT4, the level of p-Akt and attenuating the phosphorylation of IRS-1. The analysis of gene expressions of PGC-1β and Nrf-1 showed a concordance between mitochondrial DNA content in PA-induced cardiomyocytes with or without β-carotene treatment, respectively.
Conclusion:
Our results indicate that β-carotene can treat metabolic disorders by inhibition of IR pathway in diabetes.
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