Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress

Rolo, Anabela P.; Palmeira, Carlos M.

doi:10.1016/j.taap.2006.01.003

Cited by 865 publications

(620 citation statements)

References 114 publications

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“…Among mammals, the strict and accurate blood glucose control is vital because abnormal blood glucose levels can cause serious damage to health (Brownlee, 2001; Ceriello, 2003; Nathan, 1996; Rolo & Palmeira, 2006; Suh et al., 2007). However, our findings in this study are uncommon.…”

Section: Discussionmentioning

confidence: 99%

Flight is the key to postprandial blood glucose balance in the fruit batsEonycteris spelaeaandCynopterus sphinx

Peng¹,

He²,

Liu³

et al. 2017

Ecology and Evolution

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Excessive sugar consumption could lead to high blood glucose levels that are harmful to mammalian health and life. Despite consuming large amounts of sugar‐rich food, fruit bats have a longer lifespan, raising the question of how these bats overcome potential hyperglycemia. We investigated the change of blood glucose level in nectar‐feeding bats (Eonycteris spelaea) and fruit‐eating bats (Cynopterus sphinx) via adjusting their sugar intake and time of flight. We found that the maximum blood glucose level of C. sphinx was higher than 24 mmol/L that is considered to be pathological in other mammals. After C. sphinx bats spent approximately 75% of their time to fly, their blood glucose levels dropped markedly, and the blood glucose of E. spelaea fell to the fast levels after they spent 70% time of fly. Thus, the level of blood glucose elevated with the quantity of sugar intake but declined with the time of flight. Our results indicate that high‐intensive flight is a key regulator for blood glucose homeostasis during foraging. High‐intensive flight may confer benefits to the fruit bats in foraging success and behavioral interactions and increases the efficiency of pollen and seed disposal mediated by bats.

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Section: Discussionmentioning

confidence: 99%

Flight is the key to postprandial blood glucose balance in the fruit batsEonycteris spelaeaandCynopterus sphinx

Peng¹,

He²,

Liu³

et al. 2017

Ecology and Evolution

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“…They are major targets of free radical attack, 2,39 which is responsible for a variety of age-related diseases. 40,41 Further, there is accumulating evidence that during aging mitochondrial dysfunction occurs 42,43 and that age-related oxidative stress and subsequently altered gene expression may cause a dysfunction of liver metabolism. 21 This in vivo study now adds that mitochondrial dysfunction, as given by the deficiency for UCP2, elicits increased oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress-associated rise of hepatic protein glycation increases inflammatory liver injury in uncoupling protein-2 deficient mice

Kuhla

Hettwer

Menger

et al. 2010

Laboratory Investigation

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Mitochondrial dysfunction seems to be intrinsically involved in the pathogenesis of multiple organ failure because of enhanced production of reactive oxygen species and induction of oxidative damage. Chronic oxidative stress in turn causes an accumulation of advanced glycation end products (AGEs). To investigate whether mitochondrial dysfunctionassociated oxidative stress leads to increased formation and accumulation of AGE, we studied hepatic glycation in uncoupling protein-2 (UCP2À/À) knockout mice. Using the galactosamine/lipopolysaccharide (G/L)-induced liver injury model, we further tested the hypothesis that a mitochondrial dysfunction-associated increase of hepatic glycation is causative for increased liver injury. Under baseline conditions, UCP2À/À mice showed higher malondialdehyde levels and reduced glutathione/glutathione disulfide ratios as well as significantly higher hepatic levels of AGE and hepatic expression of receptor for AGE (RAGE) when compared with UCP2 þ / þ mice, indicative for increased oxidative stress and hepatic glycation. Further, livers of G/L-challenged UCP2À/À mice revealed significantly more pronounced tissue injury and were found to express higher levels of AGE and RAGE compared with wild-type mice. Functional blockade of RAGE by application of recombinant RAGE significantly diminished liver damage particularly in UCP2À/À mice. This in turn increased survival from 30% in UCP2 þ / þ mice to 50% in UCP2À/À mice. In summary, we show for the first time that mitochondrial dysfunction-associated oxidative stress enhances hepatic protein glycation, which aggravates inflammation-induced liver injury. Targeting the AGE/RAGE interaction by the blockade of RAGE might be of therapeutic value for the oxidative stress-exposed liver.

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“…Insulin secreted by beta-cells of Langerhans in pancreas, is the key hormone in the regulation of blood and tissue glucose homeostasis. Among the cluster of risk cascade in diabetes are obesity (20)(21)(22), insulin resistance (23)(24)(25)(26)(27), beta-cell dysfunction (28)(29), formation of AGEs and RAGEs, autooxidation of glucose, activation of protein kinase C, polyol pathway, hexosamine pathway, numerous intracellular metabolic disturbances (30)(31)(32) smoking (33)(34)(35)(36)(37) and genetic disposition (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Many of these abnormalities are intricately interconnected.…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species, reactive nitrogen species and antioxidants in etiopathogenesis of diabetes mellitus type-2

Singh

Mahadi

Roy

et al. 2009

Indian J Clin Biochem

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Diabetes mellitus type-2 (DMT-2) is a hyperglycemic retinopathy and embryopathy) or a-vascular (cataract and glaucoma etc). It has been proposed that all these abnormal events are initiated or activated by a common mechanism of superoxide anion, which is accompanied with generation of a variety of reactive oxygen species (ROS), reactive nitrogen specie (RNS) and resultant heightened oxidative stress (OS). Provoked OS causes IR and altered gene expressions. Hyperglycemia induces OS through multiple routes : a)stimulated polyol pathway where in d 30% glucose can be diverted to sorbitol and fructose, b)increased transcription of genes for proinflammatory cytokines and plasminogen activator inhibitor-1 (PAI-1) c) activation of protein kinase-C (PKC) leading to several molecular changes d)increased synthesis of Advanced Glycation End Products (AGEs) e)changes in a receptor far AGEs and f) autooxidation of

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Diabetes and mitochondrial function: Role of hyperglycemia and oxidative stress

Cited by 865 publications

References 114 publications

Flight is the key to postprandial blood glucose balance in the fruit batsEonycteris spelaeaandCynopterus sphinx

Flight is the key to postprandial blood glucose balance in the fruit batsEonycteris spelaeaandCynopterus sphinx

Oxidative stress-associated rise of hepatic protein glycation increases inflammatory liver injury in uncoupling protein-2 deficient mice

Reactive oxygen species, reactive nitrogen species and antioxidants in etiopathogenesis of diabetes mellitus type-2

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