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aspartic acid/obesidade

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Página 1 a partir de 39 resultados

Characterization of muscles from aspartic acid obese rats.

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This study was undertaken to determine whether changes in muscle mass, muscle fiber diameter, or shifts in fiber type occur in the aspartic acid-injected rat, an animal model of hypothalamically induced obesity. We found that diaphragm, gastrocnemius, and soleus muscle mass was 140, 149, and 171%

Aspartic acid administered neonatally affects ventilation of male and female rats differently.

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In this study ventilation was evaluated in 12-mo-old male and female rats who had received large doses of aspartic acid neonatally. Rats of both sexes treated with aspartic acid were obese, stunted, and exhibited hypogonadism. Although metabolic rates of the aspartic acid-treated rats were not

Higher intakes of energy-adjusted dietary amino acids are inversely associated with obesity risk.

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We assessed the relationship between energy-adjusted amino acids (EAA) intakes and obesity risk using data on nutrient intakes derived from the Chinese food composition tables to determine dietary intakes (DI) among 1109 obese and 3009 normal weight subjects. Dietary patterns (DP) were identified

LY226936 administered orally and centrally to obese Zucker rats suppresses food intake and body weight gain.

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LY226936, methylcarbamothoic acid-S-(4,5-dihydro-2-thiazolyl) ester, is a new compound that, when administered to obese Zucker rats, caused reduced food intake. LY226936 reduced the food consumption after a single oral dose of 50 and 100 mg/kg. On chronic oral administration to meal-fed obese (5 to

Direct evidence for the contribution of the unique I-ANOD to the development of insulitis in non-obese diabetic mice.

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Insulin-dependent diabetes mellitus is characterized by the infiltration of lymphocytes into the islets of Langerhans of the pancreas (insulitis) followed by destruction of insulin-secreting beta-cells leading to overt diabetes. The best model for the disease is the non-obese diabetic (NOD) mouse.

AMINO ACID LEVELS IN PRADER-WILLI SYNDROME AND OBESE INDIVIDUALS.

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To determine if certain features (e.g., hypopigmentation) seen in persons with Prader-Willi syndrome (PWS) may be reflected in abnormalities of amino acid metabolism, fasting plasma amino acid levels were measured from 25 patients and compared with those in 17 obese individuals. Thirteen of the
A previous genome-wide association study (GWAS) on obese/overweight Korean women reported five new genetic loci associated with the basal metabolic rate (BMR) and body mass index (BMI), NRG3, OR8U8, BCL2L2-PABPN1, PABPN1, and SLC22A17. This metabolite GWAS (mGWAS)
OBJECTIVE To investigate the association between obesity and prevalence of metabolic syndrome (MS) with its associated risk factors, in children and adolescents. METHODS A stratified random sampling method was used to select 7893 students from 6 to 18 years of age from 14 out of 396 primary and
BACKGROUND Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder frequently accompanied by obesity and by insulin resistance, and patients with this syndrome suffer from infertility and poor pregnancy outcome. Disturbances in plasma amino acid (AA) metabolism have been implicated in
Eight grossly obese children (2 girls, 8 boys, age 12.6 +/- 2.1 mean +/- SD years, mean overweight 73.3 +/- 14%) were treated for 3 weeks with a very low calorie diet (VLCD), containing 1022 kJ/240 kcal, 33 g protein, 25.5 g carbohydrate and 0.7 g fat/day. Mean weight loss after 3 weeks was 9.47 +/-
BACKGROUND Previous studies have showed differences in the amino acid (AA) composition in the plasma of people with obesity when compared to lean individuals, but the perturbations of AA concentrations in obesity and the dynamics of AA changes after weight loss is not fully understood. OBJECTIVE The
Gut microbiota play important roles in host metabolism, especially in diabetes. However, why different diets lead to similar diabetic states despite being associated with different microbiota is not clear. Mice were fed two high-energy diets (HED) with the same energy density but different

Biologically inactive leptin and early-onset extreme obesity.

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Mutations in the gene encoding leptin (LEP) typically lead to an absence of circulating leptin and to extreme obesity. We describe a 2-year-old boy with early-onset extreme obesity due to a novel homozygous transversion (c.298G→T) in LEP, leading to a change from aspartic acid to tyrosine at amino
Monogenic obesity, caused by mutations in one of the genes involved in the control of hunger and satiety, is a rare cause of early onset obesity (EOO). The most common of the single gene alterations affect the leptin gene (LEP), resulting in congenital leptin deficiency that manifests as intense

Excitotoxic lesions of the paraventricular hypothalamus: metabolic and cardiac effects.

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The excitotoxin, N-methyl-D-aspartic acid (NMDA), was used to lesion cell bodies, but not fibers-of-passage, in the paraventricular hypothalamus. Bilateral injections of NMDA (12.6 nmol/100 nl) were made into the paraventricular hypothalamus in halothane-anesthetized male Sprague-Dawley rats. Water
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