Hyperglycemia-associated alterations in cellular signaling and dysregulated mitochondrial bioenergetics in human metabolic disorders

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diabetes mellitus 2 endocrinologydiseases
diabetic foot 2 endocrinologydiseases
hyperglycemia 29 endocrinologydiseases
obesity 2 endocrinologydiseases

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diabetes mellitus 370 (pmc-release): 4/2016Publication date (ppub): /2016AbstractPurposeThe severity of untreated or refractory diabetes mellitus has been functionally linked to elevated concentrations of free plasma glucose, clinically defined as
diabetes mellitus 2846 functional dysregulation of mitochondrial bioenergetics.IntroductionThe severity of untreated or refractory diabetes mellitus has been functionally linked to elevated concentrations of free plasma glucose, clinically defined as
diabetic foot 18593 pathological states [[27], [28], [36]–[38]]. As an example, careful examination of the pathogenicity of diabetic foot ulceration, characterized by poor wound healing, will yield mechanistic links between hypoxic and hyperglycemic
diabetic foot 18858 dysfunction [[39]]. In this regard, increased hypoxic conditions leading to impaired wound healing in diabetic foot ulcerations are functionally associated with impaired hypoxia-inducible factor-1 (HIF-1) expression,
hyperglycemia 490 has been functionally linked to elevated concentrations of free plasma glucose, clinically defined as hyperglycemia . Operationally, the pathophysiological presentations of prolonged hyperglycemia may be categorized within
hyperglycemia 570 clinically defined as hyperglycemia. Operationally, the pathophysiological presentations of prolonged hyperglycemia may be categorized within insulin-dependent and insulin-independent, type 1 and type 2 diabetic phenotypes,
hyperglycemia 947 signaling systems that are significantly altered in patients presenting with diabetes-associated chronic hyperglycemia .MethodsPresently, we provide a translationally oriented review of key studies evaluating the aberrant
hyperglycemia 1074 hyperglycemia.MethodsPresently, we provide a translationally oriented review of key studies evaluating the aberrant effects of hyperglycemia on two major signaling pathways linked to debilitating cellular and systemic effects via targeted disruption
hyperglycemia 1839 II, or un-couplers of oxidative phosphorylation, were observed to significantly reduce the effects of hyperglycemia on ROS production and cellular damage, thereby establishing a critical linkage to multiple levels of
hyperglycemia 2966 has been functionally linked to elevated concentrations of free plasma glucose, clinically defined as hyperglycemia . The pathophysiological presentations of prolonged hyperglycemia may be operationally characterized
hyperglycemia 3031 plasma glucose, clinically defined as hyperglycemia. The pathophysiological presentations of prolonged hyperglycemia may be operationally characterized within insulin-dependent and insulin-independent, type 1 and type
hyperglycemia 3238 and type 2, diabetic phenotypes, respectively. Accordingly, a relatively broad spectrum of long-term hyperglycemia -associated cellular and metabolic insults has observed in diverse peripheral organ systems and central
hyperglycemia 3573 signaling systems that are significantly altered in patients presenting with diabetes-associated chronic hyperglycemia . For example, in both type 1 and type 2 diabetic patients, macro- and microvascular complications may
hyperglycemia 3935 coordinate expression of the cognate receptor for advanced glycation end-products (RAGE) [[2]]. Chronic hyperglycemia has been functionally linked to aberrant signaling processes mediated by selective enzymes of the hexosamine
hyperglycemia 4529 reductase pathway [[5]]. An overriding or unifying mechanism of diabetic pathophysiology may involve hyperglycemia -driven mitochondrial tricarboxylic acid (TCA) cycle dysregulation leading to respiratory complex III
hyperglycemia 4849 [[6]]. Presently, we coordinate parallel and convergent published studies evaluating the effects of hyperglycemia on AGEs/RAGEs, and HBP expression in relation to the pathophysiological formation of ROS, into a working
hyperglycemia 5508 hexosamine biosynthetic pathway (HBP). Additional signaling mechanisms involved in the induction of hyperglycemia -induced diabetic complications include aberrant phosphorylation events selectively mediated by protein
hyperglycemia 5768 through the aldose reductase or polyol pathway. A unifying mechanism of diabetic pathophysiology involves hyperglycemia -driven mitochondrial dysfunction and the production of high levels of ROS in the form of superoxideHyperglycemia,
hyperglycemia 7932 II, or un-couplers of oxidative phosphorylation, were observed to significantly reduce the effects of hyperglycemia on ROS production and cellular damage [[12]]. Subsequent work linked mitochondrial superoxide formation
hyperglycemia 8093 Subsequent work linked mitochondrial superoxide formation as a debilitating ROS species facilitating hyperglycemia -associated cellular damage, an effect that was reversed by overexpression of manganese superoxide dismutase
hyperglycemia 10515 incubated in the presence of hyperglycemic concentrations of glucose [[19]]. In these studies, the hyperglycemia -induced upregulation of prolyl-isomerase (Pin1) gene expression was functionally associated with nuclear
hyperglycemia 12103 transduction has been proposed as a potentially valuable therapeutic strategy for the prevention of hyperglycemia -associated cellular and vascular damage [[23]]. Notably, a genetically engineered soluble form of RAGE,
hyperglycemia 13989 signaling processes [[6]]. A key biochemical study has presented empirical evidence supporting the role of hyperglycemia -induced mitochondrial superoxide production as a strong activator of the HBP via inhibition of glyceraldehyde-3-phosphate
hyperglycemia 14595 fructose-6-phosphate aminotransferase (GFAT1) [[3]], has been proposed as a determining factor in the hyperglycemia -mediated activation of the HBP [[34]]. The molecular sequelae of aberrant HBP-mediated signaling processes
hyperglycemia 15543 selective O-GlcNAcylation of mitochondrial proteins has been explored in a preclinical model of diabetic hyperglycemia utilizing cultured cardiac myocytes [[35]]. Exposure of cultured cells to hyperglycemic conditions resulted
hyperglycemia 16217 activities of complex I, III, and restoration of normal cellular ATP concentrations. It was concluded that hyperglycemia -driven O-GlcNAcylation of selective mitochondrial proteins is functionally linked to impaired mitochondrial
hyperglycemia 17418 The deleterious biological amplification of AGEs/RAGE actions are described in the textHypoxia and hyperglycemia The etiology and persistence of major metabolic disorders afflicting diverse human populations are functionally
hyperglycemia 18200 bioenergetics and requisite ATP production.In light of the above, reciprocal pathophysiological states of hyperglycemia and hypoxia are proposed to induce significant comorbidities in human metabolic diseases. We have recently
hyperglycemia 19196 challenges. Furthermore, HIF-1 signaling has been demonstrated to be downregulated in diabetes due to hyperglycemia -induced HIF-1α destabilization linked to functional inhibition [[39]]. In sum, hyperglycemic-induced
hyperglycemia 19794 To date, advanced mitochondrial targetted therapies have not been forthcoming to address the severe hyperglycemia in concert with chronic hypoxia present in patients afflicted with type 2 diabetes.Dietary considerationsThe
hyperglycemia 20972 counteract debilitating pro-inflammatory and oxidative stress-related cellular events induced by chronic hyperglycemia have received widespread attention in the biomedical literature. Notably, supplementation with omega3-polyunsaturated
hyperglycemia 23462 pro-inflammatory processes linked to insulin resistance and hepatic dysfunction.ConclusionsProlonged periods of hyperglycemia mediate major disruptions of normative mitochondrial functions, resulting in chronic exacerbations of
hyperglycemia 23716 cellular and organ systems. As reviewed, the damaging micro- and macrovascular cellular effects of hyperglycemia are driven by mitochondrial ROS production linked to activation of parallel, but functionally convergent,
obesity 21319 peroxidation in obese and diabetic patient populations [[40]–[42]]. Accordingly, in rodent models of obesity with or without comorbid diabetes, dietary enrichment with Ω3-PUFAs was observed to reduce triglyceride
obesity 22973 comparison with those derived from Ω3-PUFAs appear to promote a higher degree of cellular damage in obesity -related comorbidities that include insulin resistance, adipose tissue inflammation [[42]], and non-alcoholic

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