Insulin and myometrial contractility; Are there any links? A narrative review.

Contrary to the evidence supporting the role for insulin in stimulating uterine contraction, only a limited number of studies have highlighted the inhibitory effect of insulin on myometrial contractions in human and rodent. A hypothetical narrative review of the current literature was conducted, revealing the current literature and shows the potential inhibitory effects of insulin on myometrial contractility. These inhibitory mechanisms include activation of adenylyl cyclase signaling pathways, an increase in cAMP production, a decrease in Ca influx and cytosolic Ca, hyperpolarization of the cell membrane, and stimulation of NO synthesis.

Increase in oxidative stress and mitochondrial impairment in hypothalamus of streptozotocin treated diabetic rat: Antioxidative effect of Withania somnifera.

Hypothalamus, the primary brain region for glucose sensing, is severely affected by oxidative stress in diabetes mellitus. Oxidative stress in this region of brain may cause severe impairment in neuronal metabolic functions. Mitochondria are prominent targets of oxidative stress and the combination of increased oxidative stress and mitochondrial dysfunctions may further decline hypothalamic neuronal functions.

Efficiency of mitochondrially targeted gallic acid in reducing brain mitochondrial oxidative damage.

Oxidative stress is associated with mitochondrial impairments. Supplying mitochondria with potent antioxidants can reduce oxidative stress—induced mitochondrial impairment. Gallic acid can be used to reduce oxidative burden in mitochondria.

Strategic localization of heart mitochondrial NOS: a review of the evidence.

Heart mitochondria play a central role in cell energy provision and in signaling. Nitric oxide (NO) is a free radical with primary regulatory functions in the heart and involved in a broad array of key processes in cardiac metabolism. Specific NO synthase (NOS) isoforms are confined to distinct locations in cardiomyocytes.

Statins lower calcium-induced oxidative stress in isolated mitochondria.

Statins are widely used cholesterol-lowering agents that exert cholesterol-independent effects including antioxidative. The present study delineates the effects of statins, atorvastatin, and simvastatin on oxidative stress and functions of mitochondria that are the primary cellular sources of oxidative stress. In isolated rat liver mitochondria, both the statins prevented calcium-induced cytochrome c release, lipid peroxidation, and opening of the mitochondrial membrane permeability transition (MPT).