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

Abstract

Background Type 2 diabetes mellitus (T2DM) is a common chronic disease that is strongly associated with cardiovascular risk. Long-term high blood glucose levels may induce cardiomyocyte apoptosis, cardiac dysfunction and suppress fetal cardiomyocyte proliferation. Recent epidemiological studies have shown a link between antioxidant carotenoids and T2DM, but a comprehensive longitudinal study of this association has not yet been conducted. Methods We included participants with biological measurements for both serum cis-β-carotene and fasting glucose from NHANES (2001–2006). We divided the participants into quartiles according to serum cis-β-carotene levels and determined the association between these levels and glucose metabolism by using multivariable regression models adjusted for confounding factors. The mechanism through which β-carotene levels regulate plasma glucose levels was further investigated in vivo and in vitro. In addition, we performed a preliminary exploration of the effects of β-carotene on diabetic rats and primary cardiomyocytes. Results Higher cis-β-carotene (quartile 4) was associated with higher LDL-cholesterol levels but lower fasting blood glucose levels. However, T2DM rats subjected to β-carotene treatment showed diminished total triglycerides and LDL-cholesterol, and their β-carotene levels were associated with better cardiac function than that in the T2DM group (P<0.05). Moreover, β-carotene was found to be an important protective factor improving cardiac and mitochondrial function in diabetes. At non-cytotoxic doses, β-carotene clearly improved glucose uptake in insulin-resistant cells. Treatment with β-carotene increased GLUT4 and p-Akt expression, and attenuated the phosphorylation of IRS-1. Our data demonstrated that β-carotene improved cardiac mitochondria biogenesis in diabetes due to activation of PGC-1β. Conclusion Our results indicate that β-carotene can be used to treat metabolic disorders through inhibition of the insulin-resistance pathway in diabetes.

Association between the dietary inflammatory index and gout in the National Health and Nutrition Examination Survey 2007–2018

“…A systematic review of dietary and nutritional contributors to the development of gout was presented by Zhang et al They found that energy-type nutritional overloads diets such as high-sugar and high-fat diets can induce hyperuricemia and inflammation, whereas adequate intake of essential nutrients is highly beneficial in gout [ 11 ]. Vitamins like vitamin A [ 39 ], vitamin D [ 40 ], and vitamin C [ 41 , 42 ] exhibit helpful anti-oxidative stress and anti-inflammatory effects with effective reduction of serum uric acid levels. Increasing the consumption of vitamins, fiber as well as unsaturated fatty acids, and supplementing with the right amount of minerals together with premium protein, can improve gout symptoms by promoting systemic metabolism [ 28 , 43 ].…”

Kynurenine‐3‐monooxygenase (KMO): From its biological functions to therapeutic effect in diseases progression

“…By reason of Wnt/β‐catenin signaling associated with lung and brain metastasis in patients with TNBC, blocking Wnt/β‐catenin pathway can inhibit breast metastasis (Krishnamurthy & Kurzrock, 2018). Moreover, KMO has been confirmed to bind to β‐catenin and the glycogen synthase kinase 3β (GSK3β) complex to reduce GSK3β kinase activity, leading to a decrease in phosphorylated β‐catenin that is susceptible to ubiquitination and degradation, thereby affecting the stability of β‐catenin (Wu et al, 2022). In general, the nonenzymatic function of KMO can promote the stability of β‐catenin and the expression of pluripotent genes, which indicate that KMO plays an important role to suppress the GSK3β kinase activity against β‐catenin (T. T. Huang, Tseng et al, 2020).…”

A multimodal therapy for infected diabetic wounds based on glucose-responsive nanocomposite-integrated microneedles

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