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sorbitol/obesità

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Pagina 1 a partire dal 48 risultati

The effect of ponalrestat on sorbitol levels in the lens of obese and diabetic mice.

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Sorbitol levels were determined in lens of genetically obese (ob/ob) and diabetic (db/db) mice, as well as in lean mice (+/db, +/ob) made diabetic by administration of streptozotocin (STZ). Treatment of lean mice with STZ resulted in hypoinsulinemia, whereas the ob/ob and db/db mice were

Role of sorbitol-mediated cellular stress response in obesity-associated retinal degeneration.

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Obesity is a global health problem associated with several diseases including ocular complications. Earlier we reported progressive retinal degeneration because of obesity in a spontaneous obese rat (WNIN/Ob) model. In the current study, we examined the molecular mechanisms leading to

Increased risk of cataract development in WNIN-obese rats due to accumulation of intralenticular sorbitol.

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Epidemiological studies have reported an association between obesity and increased incidence of ocular complications including cataract, yet the underlying biochemical and molecular mechanisms remained unclear. Previously we had demonstrated accumulation of sorbitol in the lens of obese rats
OBJECTIVE Obesity is a major public health problem worldwide, and of late, epidemiological studies indicate a preponderance of cataracts under obesity conditions. Although cataract is a multifactorial disorder and various biochemical mechanisms have been proposed, the influence of obesity on

[Comparative studies on the effect of glucose and sorbitol on the reactive increase in insulin in obesity].

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Metabolic abnormalities of the hyperglycemic obese Zucker rat.

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In a cross-sectional study, we evaluated the metabolic profiles of lean (Fa/?) and obese (fa/fa) Zucker male rats at 4 to 8 months of age. Although all of the obese rats (N = 108) demonstrated glucose intolerance, most of the obese rats exhibited only mild elevations of fasted and fed plasma
Ursolic acid (UA) is a pentacyclic triterpenoid compound that naturally occurs in fruits, leaves and flowers of medicinal herbs. This study investigated the dose-response efficacy of UA (0.01 and 0.05%) on glucose metabolism, the polyol pathway and dyslipidemia in streptozotocin/nicotinamide-induced

Fructose, xylitol, and sorbitol.

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In conclusion, fructose, sorbitol, and xylitol are calorie-containing non-glucose sugars that produce a lessened postprandial hyperglycemia in the absence of severe insulin insufficiency when given as pure substances. However, the day-long quantitative reduction of hyperglycemia that may result from

The sorbitol shunt in the retina and the optic nerve of mice with inherited and STZ-induced diabetes.

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Micromethods designed for studying the sorbitol shunt permitted studies of the retina and the optic nerve from mice. A significant accumulation of sorbitol was found in the retina of 5-months-old obese-hyper-glycaemic and severely STZ diabetic mice. The latter mice also showed increased sorbitol

[Varying utilization of glucose and sorbitol in drug-induced hypercortical metabolism].

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Utilisation of glucose and sorbitol in medically induced hypercorticalic states was investigated by means of the steroid-glucose-tolerance-test (SGTT) in 9 children, aged 6-16 years suffering from obesity and prediabetes. Prednisolone (1 mg/kg up to 20 mg) was applied 9 and 3 h prior to the loading

Use of fructose, sorbitol, or xylitol as a sweetener in diabetes mellitus.

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Non-nutritive sweeteners have been utilized in the diet of diabetic patients as agents to replace glucose and sucrose. Since saccharin might be removed from the market place, the nutritive sweeteners, fructose, xylitol, and sorbitol, are being considered as possible atlernatives. This review

Use of fructose, xylitol, or sorbitol as a sweetener in diabetes mellitus.

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Nonnutritive sweeteners have been utilized in the diet of diabetic patients an an agent to replace glucose and sucrose. Since saccharin might be removed from the marketplace, the nutritive sweeteners fructose, xylitol, and sorbitol are being considered as possible alternatives for glucose and
Insulin resistance has wide-ranging effects on metabolism but there are knowledge gaps regarding the tissue origins of systemic metabolite patterns, and how patterns are altered by fitness and metabolic health. To address these questions, plasma metabolite patterns were determined every 5 min during
OBJECTIVE Subjects with dietary obesity and pre-diabetes have an increased risk for developing both nerve conduction slowing and small sensory fiber neuropathy. Animal models of this type of neuropathy have not been described. This study evaluated neuropathic changes and their amenability to dietary

The leptin-deficient (ob/ob) mouse: a new animal model of peripheral neuropathy of type 2 diabetes and obesity.

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Whereas functional, metabolic, neurotrophic, and morphological abnormalities of peripheral diabetic neuropathy (PDN) have been extensively explored in streptozotocin-induced diabetic rats and mice (models of type 1 diabetes), insufficient information is available on manifestations and pathogenetic
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