Background: There are studies showing stimulative effect of arginine on insulin secretion. This mechanism is not fully explained. The effects of the impact of arginine on carbohydrate balance under the conditions of ischemia and reperfusion remain to be determined. The aim of this study is the evaluation of the influence of short-term L-arginine supplementation on the concentration of glucose and insulin in blood and insulin binding in rat skeletal muscle under the conditions of ischemia and reperfusion.
Methods: The study was conducted on male Wistar rats with average body mass 250 ± 30 g. Animals were divided into four groups: Group I - control, Group II - placebo, Group III - L-arginine 500 mg/kg/24 h for 5 days, Group IV - L-arginine and L-NAME (75 μmol/rat/24 h) for 5 days. Each group was divided into subgroups depending on duration of ischemia and reperfusion. Acute ischemia of hind limb was induced in each group by putting pneumatic tourniquet on the thigh. Blood samples and skeletal muscles were collected from the rats. Plasma concentrations of glucose and insulin were measured. Insulin binding to insulin receptors was determined in skeletal muscle.
Results: A clear reduction of insulin binding to receptor was found in the group of animals without ischemia and the group supplemented with L-arginine and subjected to 4-h ischemia and 30- and 120-min reperfusion. A significant increase in insulin level was found in groups of animals with L-arginine and/or L-NAME subjected to 4-h ischemia at all times of reperfusion. Supplementation with L-arginine and/or L-NAME decreased levels of glucose in blood serum of animals undergoing ischemia-reperfusion syndrome compared to the control and placebo groups.
Conclusion: Under conditions of ischemia-reperfusion, short-term administration of L-arginine causes a decrease in insulin binding capacity of insulin receptors in skeletal muscle, an increase in insulin level and a decrease in the concentration of glucose in blood serum.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/s1734-1140(12)70859-9 | DOI Listing |
Diabetes
January 2025
Nutritional Sciences and Toxicology Department, University of California Berkeley, Berkeley, CA 94720, US.
Adipocyte hypertrophy significantly contributes to insulin resistance and metabolic dysfunction. Our previous research established JMJD8 as a mediator of insulin resistance, noting its role in promoting adipocyte hypertrophy within an autonomous adipocyte context. Nevertheless, the precise mechanisms underlying this phenomenon remained elusive.
View Article and Find Full Text PDFBackground: Chronic conditions such as obesity, dyslipidemia, insulin resistance and metabolic syndrome are found with increased prevalence in older adults and are investigated as risk factors of Alzheimer's disease (AD). The exact mechanisms by which such conditions may act on the brain to promote AD pathogenesis are still unknown. We aimed to investigate the relationship between peripheral markers of metabolic function, including adiponectin, fibroblast growth factor 21 (FGF21) and insulin-like growth factor binding protein 2 (IGFBP2), and AD-associated cognitive decline.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Clinical Laboratory, Norinco General Hospital, Xi'an, Shaanxi, China.
Background: Recent studies show that N6-methyladenosine (m6A) plays an important role in the pathogenesis of the Alzheimer's disease (AD), while the mechanisms involved were studied insufficiently.
Aims: The present study aimed to explore the effect of human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2), one of the m6A-binding proteins on the progression of AD.
Materials & Methods: The mRNA and protein expression level were determined using RT-qPCR and western blot, respectively.
PNAS Nexus
January 2025
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, 3501 Fifth Avenue, Pittsburgh, PA 15261, USA.
Bronchopulmonary dysplasia, the most prevalent chronic lung disease of prematurity, is often treated with glucocorticoids (GCs) such as dexamethasone (DEX), but their use is encumbered with several adverse somatic, metabolic, and neurologic effects. We previously reported that systemic delivery of the GC prodrug ciclesonide (CIC) in neonatal rats activated glucocorticoid receptor (GR) transcriptional responses in lung but did not trigger multiple adverse effects caused by DEX. To determine whether limited systemic metabolism of CIC was solely responsible for its enhanced safety profile, we treated neonatal rats with its active metabolite desisobutyryl-ciclesonide (Des-CIC).
View Article and Find Full Text PDFBiomed Rep
March 2025
Department of Physiology, Faculty of Medicine, Maranatha Christian University, Bandung, West Java 40164, Indonesia.
Dual oxidases (DUOX) are enzymes that have the main function in producing reactive oxygen species (ROS) in various tissues. DUOX also play an important role in the synthesis of HO, which is essential for the production of thyroid hormone. Thyroid hormones can influence the process of muscle development through direct stimulation of ROS, 5' AMP-activated protein kinase (AMPK) and mTOR and indirect effect autophagy and the insulin-like growth factor 1 (IGF-1) pathway.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!