cytochrome oxidase/obesity

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Low cytochrome oxidase 4I1 links mitochondrial dysfunction to obesity and type 2 diabetes in humans and mice.

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OBJECTIVE Cytochrome oxidase (COX) dysfunction is associated with mitochondrial oxidative stress. We determined the association between COX expression, obesity and type 2 diabetes. METHODS COX4I1 and COX10 genes were measured in monocytes of 24 lean controls, 31 glucose-tolerant and 67 diabetic

Low Cytochrome Oxidase 1 Links Mitochondrial Dysfunction to Atherosclerosis in Mice and Pigs.

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BACKGROUND Cytochrome oxidase IV complex regulates energy production in mitochondria. Therefore, we determined the relation of COX genes with atherosclerosis in mice and pigs. RESULTS First, we compared atherosclerosis in the aortic arch of age-matched (24 weeks) C57BL/6J control (n = 10),

Mechanisms of the antidiabetic effects of the beta 3-adrenergic agonist CL-316243 in obese Zucker-ZDF rats.

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Previous studies have demonstrated that chronic cold exposure activates the sympathetic nervous system, increases energy expenditure, improves glucose uptake in peripheral tissues [brown and white adipose tissues (BAT and WAT) and muscles] of normal rats. The goal of the present studies was to test

Studies on the activity of brown adipose tissue in suckling, pre-obese, ob/ob mice.

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The properties and activity of brown adipose tissue have been investigated in suckling, pre-obese, ob/ob mice in order to determine whether decreased thermogenesis in the tissue precedes the development of obesity in this mutant. At 14 days of age there was no difference between the ob/ob and normal

Neuronal activity in hypothalamic nuclei of obese and lean Zucker rats.

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Central neural activity was assessed by measuring relative cytochrome oxidase (CO) activity in the ventromedial nucleus (VMN; thermogenesis regulation), the parvocellular paraventricular nucleus (PVN; feeding regulation), and the magnocellular PVN (secretion of vasopressin and oxytocin) in 10

Impaired diet-induced thermogenesis in brown adipose tissue from rats made obese with parasagittal hypothalamic knife-cuts.

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Two experiments were performed to determine if bilateral parasagittal hypothalamic knife-cuts (KCs), which produce long-term overeating and obesity, after biochemical indices of brown adipose tissue (BAT) reactivity to thermogenic stimuli. In the first study, responses to environmental cold were

Mechanism linking insulin resistance to defective thermogenesis in brown adipose tissue of obese diabetic SHR/N-cp rats.

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We previously reported that the decreased sensitivity of brown adipose tissue (BAT) from obese Zucker rats to the calorigenic effects of norepinephrine is associated with a marked resistance to insulin, and we suggested that this defect may explain, at least in part, the increased energy gain

Exercise training and clenbuterol reduce insulin resistance of obese Zucker rats.

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This study compared the effects of aerobic exercise training and chronic administration of the selective beta 2-adrenergic agonist clenbuterol on whole body and skeletal muscle insulin resistance in obese (fa/fa) Zucker rats. Obese rats were randomly assigned to training, clenbuterol, or sedentary

Brown adipose tissue in genetically obese (fa/fa) rats: response to cold and diet.

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Young genetically obese (fatty, fa/fa) rats (7-8 wk old) maintained on a chow diet at 28 degrees C have a relatively normal amount of brown adipose tissue (BAT) (normal protein content, normal noradrenaline content, normal or slightly reduced cytochrome oxidase content, 30% reduction in DNA content)

Downregulation of PGC-1α Prevents the Beneficial Effect of EET-Heme Oxygenase-1 on Mitochondrial Integrity and Associated Metabolic Function in Obese Mice.

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Background/Objectives. Obesity and metabolic syndrome and associated adiposity are a systemic condition characterized by increased mitochondrial dysfunction, inflammation, and inhibition of antioxidant genes, HO-1, and EETs levels. We postulate that EETs attenuate adiposity by stimulating

Effects of hypoxic living and training on gene expression in an obese rat model.

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OBJECTIVE The study's purpose was to determine in a rat obesity model the effects of normoxic training, sedentary hypoxic living, or hypoxic living plus training on the skeletal muscle messenger RNA (mRNA) levels of 14 genes involved in oxygen sensing (hypoxia-inducible factor 1α, vascular

Specific decrease of mitochondrial thermogenic capacity in brown adipose tissue of obese SHR/N-cp rats.

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The metabolic properties of brown adipose tissue (BAT), liver, and skeletal muscles were compared in lean and obese diabetic SHR/N-cp rats (a new model of type II diabetes) to test whether the severe insulin resistance of obese animals is specifically associated with a thermogenic defect in BAT. The

Liver mitochondrial properties from the obesity-resistant Lou/C rat.

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OBJECTIVE The first objective was to evaluate the influence of caloric intake on liver mitochondrial properties. The second objective was aimed at determining the impact of increasing fat intake on these properties. METHODS Lou/C rats, displaying an inborn low caloric intake and resistant to

Muscle morphological and biochemical adaptations to training in obese Zucker rats.

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The purposes of the present study were to characterize the histochemical and enzymatic profiles of various hindlimb skeletal muscles, as well as to determine maximal O2 consumption (VO2max) and respiratory exchange ratios (R) during steady-state exercise in the obese Zucker rat. The changes that

Effects of exercise training on brown adipose tissue thermogenesis in ovariectomized obese rats.

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The effect of exercise training on brown adipose tissue (BAT) thermogenesis was studied by measuring cytochrome oxidase activity, as a marker of mitochondrial abundance, mitochondrial guanosine-5'-diphosphate (GDP) binding, as an indicator of thermogenic activity and oxygen consumption in BAT in

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