huntington disease/carbohydrate

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Exaggerated growth hormone response to arginine infusion in Huntington's disease.

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Growth hormone regulation was studied in 10 patients with Huntington's disease after intravenous administration of arginine. In 20 control subjects arginine infusion resulted in a rise of plasma growth hormone levels from a mean baseline value of 3.2+/-0.6 ng/ml to a peak level of 17.6+/-2.7 ng/ml

Material prepared from normal brain inhibits migration of leukocytes from Huntington's disease patients.

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Material inhibiting migration of leukocytes in vitro from Huntington's disease patients, was obtained from human brain removed at autopsy. The active material was present in brainstem, basal ganglia and cerebellum but not in cerebral cortex. It could be recovered at autopsy up to 21.5 h after death,

Metabolic impairment and membrane abnormality in red cells from Huntington's disease.

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The following aspects have been investigated in 10 patients affected by Huntington's disease )HD): --extensive haematological investigations; --red cell enzyme activities and level of the most important glycolytic intermediate compounds; --protein, lipid and carbohydrate composition of the

Endogenous sodium-potassium ATPase inhibition related biochemical cascade in trisomy 21 and Huntington's disease: neural regulation of genomic function.

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The isoprenoid pathway related cascade was assessed in trisomy 21 and Huntington's disease. Membrane Na+-K+ ATPase activity, serum magnesium and ubiquinone were decreased while HMG CoA reductase activity, serum digoxin and dolichol levels were increased in both the disorders. There were increased

Metabolite mapping reveals severe widespread perturbation of multiple metabolic processes in Huntington's disease human brain.

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Huntington's disease (HD) is a genetically-mediated neurodegenerative disorder wherein the aetiological defect is a mutation in the Huntington's gene (HTT), which alters the structure of the huntingtin protein (Htt) through lengthening of its polyglutamine tract, thus initiating a cascade that

A Metabolic Study of Huntington's Disease.

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BACKGROUND Huntington's disease patients have a number of peripheral manifestations suggestive of metabolic and endocrine abnormalities. We, therefore, investigated a number of metabolic factors in a 24-hour study of Huntington's disease gene carriers (premanifest and moderate stage II/III) and

Mechanism(s) of alteration of micro RNA expressions in Huntington's disease and their possible contributions to the observed cellular and molecular dysfunctions in the disease.

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To identify the mechanism of deregulation of micro RNAs (miRNAs) altered in Huntington's disease (HD) and their possible contributions to the altered cellular and molecular functions observed in the disease, we analyzed the altered miRNAs in the postmortem brains of HD patients. There are 54 miRNAs

A ketogenic diet delays weight loss and does not impair working memory or motor function in the R6/2 1J mouse model of Huntington's disease.

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Ketogenic diets are high in fat and low in carbohydrates, and have long been used as an anticonvulsant therapy for drug-intractable and pediatric epilepsy. Additionally, ketogenic diets have been shown to provide neuroprotective effects against acute and chronic brain injury, including beneficial

Abnormal glucose tolerance and arginine tolerance tests in Huntington's disease.

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Neuropathological studies of Huntington's disease reveal neuronal atrophy, lipofuscin accumulation and other findings characteristic of the aged brain, although the onset of disease is only the fourth decade. The pathology is limited to specific areas such as the caudate nucleus, cerebral cortex and

Nutritional evaluation of Huntington disease patients.

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A nutritional survey and evaluation was made in Huntington disease patients by the 24-h-recall method. Control subjects and choreic patients consumed a diet that supplied all the essential amino acids. The diet was hypocaloric, rich in animal protein, and low in fat and carbohydrates. The ratio of

Altered lipid metabolism in Drosophila model of Huntington's disease.

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Huntington's disease (HD) is late-onset, progressive neurodegenerative disorder caused by expansion of polyglutamine (polyQ) repeat within Huntingtin (Htt) protein. In HD patients, energy-related manifestations such as modulation of weight during entire course of disease with energy deficit at

Diabetes mellitus in Huntington disease.

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There have been conflicting reports that individuals with Huntington disease (HD) are prone to abnormalities of carbohydrate metabolism. In this study information about the incidence and control of diabetes mellitus in 620 probands (278 living, 332 deceased) with HD and in their first and second

Peripheral Expression of Mutant Huntingtin is a Critical Determinant of Weight Loss and Metabolic Disturbances in Huntington's Disease.

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Deteriorating weight loss in patients with Huntington's disease (HD) is a complicated peripheral manifestation and the cause remains poorly understood. Studies suggest that body weight strongly influences the clinical progression rate of HD and thereby offers a valuable target for therapeutic

Mechanistically linking age-related diseases and dietary carbohydrate via autophagy and the ubiquitin proteolytic systems.

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Epidemiological data indicate that consuming diets that deliver sugar to the blood rapidly (called high glycemic index, GI) is associated with enhanced risk for age-related diseases such as cardiovascular disease, type 2 diabetes, cataract and age-related macular degeneration (AMD). These debilities

Expression of the CD15 epitope in the human magnocellular basal forebrain system.

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The distribution of the carbohydrate epitope 3-fucosyl-N-acetyl-lactosamine (CD15) has been immunocytochemically evaluated in coronal paraffin sections through the magnocellular basal forebrain system--the nucleus basalis of Meynert, the nucleus of the diagonal band of Broca and the medial septal

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