Stress adaptation is associated with insulin resistance in women with gestational diabetes mellitus

Feng, Yan; Feng, Qi; Qu, Hongmei; Song, Xuejing; Hu, Jianwei; Xu, Xiaomeng; Zhang, Li; Yin, Shanshan

doi:10.1038/s41387-020-0107-8

Cited by 35 publications

(25 citation statements)

References 27 publications

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“…Stress-induced inflammation may cause the development of insulin resistance [ 65 , 66 , 67 ]. Stress activates the hypothalamic–pituitary–adrenal axis, renin–angiotensin system pathway, and sympathoadrenal system, all of which are involved in the production of pro-inflammatory cytokines, resulting in the negative downregulation of insulin signaling by either phosphorylating insulin resistance serine residues or inhibiting Akt, resulting in insulin resistance.…”

Section: Ca Vs Hyperglycemia and Insulin Resistancementioning

confidence: 99%

Caffeic Acid on Metabolic Syndrome: A Review

et al. 2021

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Metabolic syndrome (MetS) is a constellation of risk factors that may lead to a more sinister disease. Raised blood pressure, dyslipidemia in the form of elevated triglycerides and lowered high-density lipoprotein cholesterol, raised fasting glucose, and central obesity are the risk factors that could lead to full-blown diabetes, heart disease, and many others. With increasing sedentary lifestyles, coupled with the current COVID-19 pandemic, the numbers of people affected with MetS will be expected to grow in the coming years. While keeping these factors checked with the polypharmacy available currently, there is no single strategy that can halt or minimize the effect of MetS to patients. This opens the door for a more natural way of controlling the disease. Caffeic acid (CA) is a phytonutrient belonging to the flavonoids that can be found in abundance in plants, fruits, and vegetables. CA possesses a wide range of beneficial properties from antioxidant, immunomodulatory, antimicrobial, neuroprotective, antianxiolytic, antiproliferative, and anti-inflammatory activities. This review discusses the current discovery of the effect of CA against MetS.

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Section: Ca Vs Hyperglycemia and Insulin Resistancementioning

confidence: 99%

Caffeic Acid on Metabolic Syndrome: A Review

et al. 2021

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“…IR is closely associated with reduced oxidative stress in GMD. Oxidative stress is considered to be involved in the induction of IR ( 30 – 32 ). Therefore, TrxR1 can decrease IR by suppressing oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

miR‑875‑5p regulates IR and inflammation via targeting TXNRD1 in gestational diabetes rats

et al. 2021

Mol Med Rep

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Gestational diabetes mellitus (GdM) is a serious life-threatening disease that affects the mother and fetus. However, the pathogenesis of GdM is still unclear. micrornas (mirs) play vital roles in the regulation of various cell functions. The present study aimed to investigate the effects of mir-875-5p and thioredoxin reductase 1 cytoplasmic (TXnrd1) in GdM rats and analyze the associated underlying mechanism. a GdM rat model was induced using an intraperitoneal injection of streptozotocin. mir-875-5p knockdown plasmids or TXnrd1 knockdown plasmids were injected into the rats via the caudal vein. mir-875-5p and TXnrd1 expression in the serum were detected using reverse transcription-quantitative Pcr (rT-qPcr) or western blot (WB) analyses. The fasting blood-glucose (FBG), fasting serum insulin, triglyceride and high density lipoprotein levels were detected by specific commercial kits. The inflammatory response and the induction of oxidative stress were analyzed by assessing the expression of associated markers via WB, rT-qPcr or commercial kits. The pancreatic and placental injuries were detected by hematoxylin and eosin staining. The results indicated that mir-875-5p expression levels were downregulated, whereas TXnrd1 levels were upregulated in GdM rats compared with normal pregnancy rats. mir-875-5p significantly regulated TXnrd1 expression in GdM rats. mir-875-5p silencing notably reduced FBG and insulin resistance, which was accompanied by reduced expression levels of blood lipid and pro-inflammatory markers as well as reduced oxidative stress. However, the effects of mir-875-5p could be reversed by TXnrd1 silencing. Therefore, the present study indicated that miR-875-5p regulated IR and inflammation by targeting TXnrd1 in GdM rats. mir-875-5p and TXnrd1 may be considered as potential targets for treating GdM.

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“…This suggests that uterine artery CSE deficiency could promote preeclampsia via higher oxidative stress and eNOS inactivation. Furthermore, diabetes is a preeclampsia risk factor associated with decreased serum GSH and elevated serum homocysteine [ 64 , 65 ]; homocysteine may increase vascular stiffness in post-menopausal women as well [ 66 ]. Hyperglycemia also suppresses CSE protein expression in hepatocytes and peripheral blood mononuclear cells [ 67 ].…”

Section: Discussionmentioning

confidence: 99%