The Liver, Glucose Homeostasis, and Insulin Action in Type 2 Diabetes Mellitus

Radziuk, J.; Pye, Susan

doi:10.1007/978-1-60327-116-5_18

Cited by 1 publication

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“…Due to its strategic position, between the intestinal bed and the systemic circulation, the liver was regarded as buffer organ for the regulation of metabolic fluxes [ 5 , 6 ]. As glucose and fatty acid metabolisms are largely dependent on mitochondria to generate energy in cells, any impairment in nutrients oxidation, together with a reduced mitochondrial content, could thereby establish a vicious cycle of metabolic alterations involved in the pathogenesis of T2DM, leading to an increased generation of free radicals.…”

Section: Introductionmentioning

confidence: 99%

Hepatic Mitochondrial Alterations and Increased Oxidative Stress in Nutritional Diabetes-PronePsammomys obesusModel

Bouderba

Sanz

Sánchez-Martín

et al. 2012

Experimental Diabetes Research

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Mitochondrial dysfunction is considered to be a pivotal component of insulin resistance and associated metabolic diseases. Psammomys obesus is a relevant model of nutritional diabetes since these adult animals exhibit a state of insulin resistance when fed a standard laboratory chow, hypercaloric for them as compared to their natural food. In this context, alterations in bioenergetics were studied. Using liver mitochondria isolated from these rats fed such a diet for 18 weeks, oxygen consumption rates, activities of respiratory complexes, and content in cytochromes were examined. Levels of malondialdehyde (MDA) and gluthatione (GSH) were measured in tissue homogenates. Diabetic Psammomys showed a serious liver deterioration (hepatic mass accretion, lipids accumulation), accompanied by an enhanced oxidative stress (MDA increased, GSH depleted). On the other hand, both ADP-dependent and uncoupled respirations greatly diminished below control values, and the respiratory flux to cytochrome oxydase was mildly lowered. Furthermore, an inhibition of complexes I and III together with an activation of complex II were found. With emergence of oxidative stress, possibly related to a defect in oxidative phosphorylation, some molecular adjustments could contribute to alleviate, at least in part, the deleterious outcomes of insulin resistance in this gerbil species.

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Section: Introductionmentioning

confidence: 99%