International Journal of Molecular Sciences

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Dear Colleagues,

Metabolic syndrome (MS) is a group of signs that increase the risk of developing type 2 diabetes mellitus, cardiovascular diseases, and certain types of cancer. At least three signs must be present: central obesity, hypertension, dyslipidemia, insulin resistance, hyperinsulinemia, high fasting glucose, and altered glucose tolerance. Insulin resistance is a defect in insulin signaling that impairs the effects of this hormone, resulting in fasting and postprandial hyperinsulinemia and increased glucose levels.

Defects in the insulin signaling pathway include insulin binding to the insulin receptor (IR), which induces conformational changes that lead to the transphosphorylation of the beta subunits of IR and tyrosine kinase activity that begin with a cascade of phosphorylation of other IR-recruited proteins. The next protein recruited is the insulin receptor substrate (IRS), which mediates most of the insulin intracellular signaling, alongside other scaffold proteins and sequential phosphorylations that can be affected by insulin resistance. We can name phosphatidylinositol 3-kinase (PI3K), protein kinase C (PKC), phosphoinositide-dependent kinase (PDK), the PKB/Akt pathway, mTOR-related protein synthesis, FOXO1 and sterol regulatory element-binding protein SREBP, and the translocation of GLUT4 to the membrane. Many mechanisms have been described to explain IR. However, it is interesting to discuss the molecular mechanisms that link metabolic syndrome and the resistance of sensitive tissues to this hormone.

Dr. Marcia Hiriart
Guest Editor

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Keywords

metabolic syndrome
insulin resistance
IRS
protein phosphorylation
insulin receptor
AKT
mTOR

Published Papers (2 papers)

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Research

14 pages, 3153 KiB

Open AccessArticle

Ancistrocladus tectorius Extract Inhibits Obesity by Promoting Thermogenesis and Mitochondrial Dynamics in High-Fat Diet-Fed Mice

by Minju Kim, Jin Hyub Paik, Hwa Lee, Min Ji Kim, Sang Mi Eum, Soo Yong Kim, Sangho Choi, Ho-Yong Park, Hye Gwang Jeong and Tae-Sook Jeong

Int. J. Mol. Sci. 2024, 25(7), 3743; https://doi.org/10.3390/ijms25073743 - 27 Mar 2024

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Abstract

Root extracts of Ancistrocladus tectorius (AT), a shrub native to China, have been shown to have antiviral and antitumor activities, but the anti-obesity effects of AT aerial parts, mainly the leaves and stems, have not been investigated. This study is the first to investigate the anti-obesity effects and molecular mechanism of AT 70% ethanol extract in 3T3-L1 adipocytes and high-fat diet (HFD)-fed C57BL/6J mice. Treatment with AT extract inhibited lipid accumulation in 3T3-L1 cells and decreased the expression of adipogenesis-related genes. AT extract also upregulated the mRNA expression of genes related to mitochondrial dynamics in 3T3-L1 adipocytes. AT administration for 12 weeks reduced body weight and organ weights, including liver, pancreas, and white and brown adipose tissue, and improved plasma profiles such as glucose, insulin, homeostasis model assessment of insulin resistance, triglyceride (TG), and total cholesterol in HFD-fed mice. AT extract reduced HFD-induced hepatic steatosis with levels of liver TG and lipogenesis-related genes. AT extract upregulated thermogenesis-related genes such as Cidea, Pgc1α, Ucp1, Prdm16, Adrb1, and Adrb3 and mitochondrial dynamics-related genes such as Mff, Opa1, and Mfn2 in brown adipose tissue (BAT). Therefore, AT extract effectively reduced obesity by promoting thermogenesis and the mitochondrial dynamics of BAT in HFD-fed mice. Full article

(This article belongs to the Special Issue Insulin Resistance and Metabolic Syndrome)

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20 pages, 3846 KiB

Open AccessArticle

Sex Modulates Response to Renal-Tubule-Targeted Insulin Receptor Deletion in Mice

by Soha Sohail, Gabriella Akkawi, Taylor Rechter, Maurice B. Fluitt and Carolyn M. Ecelbarger

Int. J. Mol. Sci. 2023, 24(9), 8056; https://doi.org/10.3390/ijms24098056 - 29 Apr 2023

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Abstract

Insulin facilitates renal sodium reabsorption and attenuates gluconeogenesis. Sex differences in this regulation have not been well characterized. Using tetracycline-inducible Cre-lox recombination, we knocked out (KO) the insulin receptor (InsR) from the renal tubule in adult male (M) and female (F) mice (C57Bl6 background) with a paired box 8 (PAX8) promoter. Body weights were not affected by the KO, but mean kidney weights were reduced in the KO mice (13 and 3%, in M and F, respectively, relative to wild-type (WT) mice). A microscopic analysis revealed 25 and 19% reductions in the proximal tubule (PT) and cortical collecting duct cell heights, respectively, in KOMs relative to WTMs. The reductions were 5 and 11% for KOFs. Western blotting of renal cortex homogenates showed decreased protein levels for the β and γ subunits of the epithelial sodium channel (ENaC) and the sodium-potassium-2-chloride cotransporter type 2 (NKCC2) in both sexes of KO mice; however, α-ENaC was upregulated in KOMs and downregulated in KOFs. Both sexes of KO mice cleared exogenously administered glucose faster than the WT mice and had lower semi-fasted, anesthetized blood glucose levels. However, KOMs (but not KOFs) demonstrated evidence of enhanced renal gluconeogenesis, including higher levels of renal glucose-6-phosphatase, the PT’s production of glucose, post-prandial blood glucose, and plasma insulin, whereas KOFs exhibited downregulation of renal high-capacity sodium glucose cotransporter (SGLT2) and upregulation of SGLT1; these changes appeared to be absent in the KOM. Overall, these findings suggest a sex-differential reliance on intact renal tubular InsR signaling which may be translationally important in type 2 diabetes, obesity, or insulin resistance when renal insulin signaling is reduced. Full article

(This article belongs to the Special Issue Insulin Resistance and Metabolic Syndrome)

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