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Anti-insulin resistance effects of salidroside through mitochondrial quality control.

07:00 EST 1st December 2019 | BioPortfolio

Summary of "Anti-insulin resistance effects of salidroside through mitochondrial quality control."

Mitochondrial quality control (MQC) and function are determinants for cellular energy metabolism and their disorders are reported to play important role in the development of insulin resistance (IR). Salidroside was reported to have beneficial effects on MQC through AMPK pathway, however, it is unknown whether salidroside exerts anti-IR effect with this action. This study sought to investigate effects of salidroside on IR with an exploration of the mechanisms of its action. Experimental IR models were adopted in high-fat diet (HFD) fed mice and palmitate-treated C2C12 myotubes, respectively. Blood levels of glucose and insulin as well as cellular glucose uptake were determined, mitochondrial function and MQC-associated parameters and reactive oxygen species (ROS) production were analyzed based on treatments with activator (AICAR), inhibitors (compound C and EX-527), or specific siRNA of AMPK/SIRT1 and mitochondrial ROS scavenger (mito-TEMPO). Protein expression level was determined by Western-Blot, cellular observation by transmission electron microscope, and ROS production by functional analysis kits. Salidroside reduced IR and activated insulin signaling along with stimulation of AMPK/SIRT1 signaling and downstream regulation of MQC and ROS production. These salidroside effects were comparable to those of AICAR and could be prevented by AMPK/SIRT1 inhibitors or siRNAs, respectively. Salidroside reduces IR and regulates MQC and ROS production through activating AMPK/SIRT1 signaling pathway. Since IR is a critical issue for public health, to explore a potent agent against IR is of high interest. The anti-IR effects of salidroside warrant further experimental and clinical studies.

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This article was published in the following journal.

Name: The Journal of endocrinology
ISSN: 1479-6805
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A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.

Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS. It can be caused by the presence of INSULIN ANTIBODIES or the abnormalities in insulin receptors (RECEPTOR, INSULIN) on target cell surfaces. It is often associated with OBESITY; DIABETIC KETOACIDOSIS; INFECTION; and certain rare conditions. (from Stedman, 25th ed)

THIAZOLES with two keto oxygens. Members are insulin-sensitizing agents which overcome INSULIN RESISTANCE by activation of the peroxisome proliferator activated receptor gamma (PPAR-gamma).

Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.

Rare autosomal recessive syndrome of extreme insulin resistance due to mutations in the binding domain of INSULIN RECEPTOR. Clinical features include severe intrauterine and postnatal growth restriction, characteristic dysmorphic FACIES; HIRSUTISM; VIRILIZATION; multiple endocrine abnormalities, and early death.

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