Gender discrimination in the influence of hyperglycemia and hyperosmolarity on rat aortic tissue responses to insulin

Wong, Nikki; Achike, Francis I.

doi:10.1016/j.regpep.2010.04.003

Cited by 3 publications

(5 citation statements)

References 25 publications

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“…Adiponectin shows a sexual dimorphism, with levels higher in females than males, and it attenuates the pathophysiological processes leading to disease states such as T2DM, obesity, atherosclerosis, metabolic syndrome and non‐alcoholic fatty liver disease 51,56 . It is possible that adiponectin is one of the factors conferring the well‐known advantage to females in terms of the development of cardiovascular disease 57 . From a therapeutic viewpoint, adiponectin has been shown to enhance energy expenditure in animal models, but not in humans 58 and PPAR antagonists stimulate adiponectin levels in addition to potentiating the effects of leptin 50 …”

Section: Adipose Tissue and Hormonesmentioning

confidence: 99%

“…51,56 It is possible that adiponectin is one of the factors conferring the well-known advantage to females in terms of the development of cardiovascular disease. 57 From a therapeutic viewpoint, adiponectin has been shown to enhance energy expenditure in animal models, but not in humans 58 and PPAR antagonists stimulate adiponectin levels in addition to potentiating the effects of leptin. 50…”

Section: Adipose Tissue and Hormonesmentioning

confidence: 99%

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Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint

Achike

Wang

et al. 2010

Clin Exp Pharma Physio

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SUMMARY1. Obesity is a metabolic disease of pandemic proportions largely arising from positive energy balance, a consequence of sedentary lifestyle, conditioned by environmental and genetic factors. Several central and peripheral neurohumoral factors (the major ones being the anorectic adipokines leptin and adiponecin and the orexigenic gut hormone ghrelin) acting on the anorectic (pro-opiomelanocortin and cocaine-and amphetamine-regulated transcript) and orexigenic (neuropeptide Y and agouti generelated protein) neurons regulate energy balance. These neurons, mainly in the arcuate nucleus of the hypothalamus, project to parts of the brain modulating functions such as wakefulness, autonomic function and learning. A tilt in the anorectic-orexigenic balance, perhaps determined genetically, leads to obesity.2. Excess fat deposition requires space, created by adipocyte (hypertrophy and hyperplasia) and extracellular matrix (ECM) remodelling. This process is regulated by several factors, including several adipocyte-derived Matrix metalloproteinases and the adipokine cathepsin, which degrades fibronectin, a key ECM protein. Excess fat, also deposited in visceral organs, generates chronic low-grade inflammation that eventually triggers insulin resistance and the associated comorbidities of metabolic syndrome (hypertension, atherosclerosis, dyslipidaemia and diabetes mellitus).3. The perivascular adipose tissue (PVAT) has conventionally been considered non-physiological structural tissue, but has recently been shown to serve a paracrine function, including the release of adipose-derived relaxant and contractile factors, akin to the role of the vascular endothelium. Thus, PVAT regulates vascular function in vivo and in vitro, contributing to the cardiovascular pathophysiology of the metabolic syndrome. Defining the mechanism of PVAT regulation of vascular reactivity requires more and better controlled investigations than currently seen in the literature.

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Section: Adipose Tissue and Hormonesmentioning

confidence: 99%

Section: Adipose Tissue and Hormonesmentioning

confidence: 99%

Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint

Achike

Wang

et al. 2010

Clin Exp Pharma Physio

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“…Human studies also supports the concept that women who progressed from normoglycemia to pre-diabetes or hyperglycemia have a greater endothelial dysfunction, more hypertension, and a greater degree of fibrinolysis/thrombosis than men [7]. However, mechanisms by which diabetes impacts more female than male remain unclear [6,7]. …”

Section: Introductionmentioning

confidence: 96%

“…For instance, animal studies showed that endothelium-intact thoracic aortic rings from age-matched male and female Sprague–Dawley rats were responsive to insulin, by showing the relaxation. The hyperglycemia was found able to inhibit the response of aortic rings to insulin and apparently the female vascular endothelium is more sensitive to the toxic effect of hyperglycemia than the male vascular endothelium [6]. Human studies also supports the concept that women who progressed from normoglycemia to pre-diabetes or hyperglycemia have a greater endothelial dysfunction, more hypertension, and a greater degree of fibrinolysis/thrombosis than men [7].…”

Section: Introductionmentioning

confidence: 97%

Zinc protects against diabetes-induced pathogenic changes in the aorta: roles of metallothionein and nuclear factor (erythroid-derived 2)-like 2

Miao

Wang

Sun

et al. 2013

Cardiovasc Diabetol

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BackgroundCardiovascular diseases remain a leading cause of the mortality world-wide, which is related to several risks, including the life style change and the increased diabetes prevalence. The present study was to explore the preventive effect of zinc on the pathogenic changes in the aorta.MethodsA genetic type 1 diabetic OVE26 mouse model was used with/without zinc supplementation for 3 months. To determine gender difference either for pathogenic changes in the aorta of diabetic mice or for zinc protective effects on diabetes-induced pathogenic changes, both males and females were investigated in parallel by histopathological and immunohistochemical examinations, in combination of real-time PCR assay.ResultsDiabetes induced significant increases in aortic oxidative damage, inflammation, and remodeling (increased fibrosis and wall thickness) without significant difference between genders. Zinc treatment of these diabetic mice for three months completely prevented the above pathogenic changes in the aorta, and also significantly up-regulated the expression and function of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a pivotal regulator of anti-oxidative mechanism, and the expression of metallothionein (MT), a potent antioxidant. There was gender difference for the protective effect of zinc against diabetes-induced pathogenic changes and the up-regulated levels of Nrf2 and MT in the aorta.ConclusionsThese results suggest that zinc supplementation provides a significant protection against diabetes-induced pathogenic changes in the aorta without gender difference in the type 1 diabetic mouse model. The aortic protection by zinc against diabetes-induced pathogenic changes is associated with the up-regulation of both MT and Nrf2 expression.

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“…The aortic rings were pretreated with 10 −4 M L-NAME to denudate the endothelium chemically and thus to assess only the vasoconstrictive responses of vascular smooth muscle. For the HG condition, the total glucose concentration in each chamber was adjusted to 25 mM [ 40 ] or 50 mM [ 41 ] for 30 min. Mannitol was used to prepare a high osmolarity control corresponding to HG50.…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rb1 Reduces Hyper-Vasoconstriction Induced by High Glucose and Endothelial Dysfunction in Rat Aorta

Park,

Shin,

Kim

et al. 2023

Pharmaceuticals

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Acute hyperglycemia induces oxidative damage and inflammation, leading to vascular dysfunction. Ginsenoside Rb1 (Rb1) is a major component of red ginseng with anti-diabetic, anti-oxidant and anti-inflammatory properties. Here, we investigated the beneficial effects and the underlying mechanisms of Rb1 on hypercontraction induced by high glucose (HG) and endothelial dysfunction (ED). The isometric tension of aortic rings was measured by myography. The rings were treated with NG-nitro-L-arginine methyl ester (L-NAME) to induce chemical destruction of the endothelium, and Rb1 was added after HG induction. The agonist-induced vasoconstriction was significantly higher in the aortic rings treated with L-NAME + HG50 than in those treated with HG50 or L-NAME (p = 0.011) alone. Rb1 significantly reduced the hypercontraction in the aortic rings treated with L-NAME + HG50 (p = 0.004). The ATP-sensitive K+ channel (KATP) blocker glibenclamide tended to increase the Rb1-associated reduction in the agonist-induced vasoconstriction in the rings treated with L-NAME + HG50. The effect of Rb1 in the aortic rings treated with L-NAME + HG50 resulted from a decrease in extracellular Ca2+ influx through the receptor-operated Ca2+ channel (ROCC, 10−6–10−4 M CaCl2, p < 0.001; 10−3–2.5 × 10−3 M CaCl2, p = 0.001) and the voltage-gated Ca2+ channel (VGCC, 10−6 M CaCl2, p = 0.003; 10−5–10−2 M CaCl2, p < 0.001), whereas Rb1 did not interfere with Ca2+ release from the sarcoplasmic reticulum. In conclusion, we found that Rb1 reduced hyper-vasoconstriction induced by HG and ED by inhibiting the ROCC and the VGCC, and possibly by activating the KATP in rat aorta. This study provides further evidence that Rb1 could be developed as a therapeutic target for ED in diabetes.

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Gender discrimination in the influence of hyperglycemia and hyperosmolarity on rat aortic tissue responses to insulin

Cited by 3 publications

References 25 publications

Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint

Obesity, metabolic syndrome, adipocytes and vascular function: A holistic viewpoint

Zinc protects against diabetes-induced pathogenic changes in the aorta: roles of metallothionein and nuclear factor (erythroid-derived 2)-like 2

Ginsenoside Rb1 Reduces Hyper-Vasoconstriction Induced by High Glucose and Endothelial Dysfunction in Rat Aorta

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