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hyperinsulinism/gojaznost
Veza se sprema u međuspremnik
Page 1 od 5098 rezultati
Hyperinsulinemia and abdominal obesity are more prevalent in non-diabetic subjects with family history of type 2 diabetes.
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BACKGROUND
This study was undertaken in order to identify the relationships between family history of type 2 diabetes and cardiovascular risk factors in non-diabetic Mexican individuals.
METHODS
The design was a cross-sectional, population-based study stratified by age and sex. Participants
Basal and growth hormone-induced hepatic messenger ribonucleic acid expression of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3 is independent of hyperinsulinemia and increased energy status in the genetically obese Zucker rat.
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Genetically obese Zucker rats, like obese humans, have normal or elevated circulating insulin-like growth factor-I (IGF-I) levels in the presence of low GH secretion. Hyperinsulinemia, increased energy status, or other nutritional factors associated with obesity could be responsible for these
Alterations of glucoregulation in childhood obesity--association with insulin resistance and hyperinsulinemia.
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OBJECTIVE
To study the prevalence of alterations of glucoregulation in childhood obesity.
METHODS
250 obese children. Oral glucose tolerance test was performed, serum glucose and insulin were determined, and HOMA-IR was calculated.
RESULTS
Impaired fasting glucose (IFG) was found in 1.2% according
Hyperinsulinemia in obesity syndromes: its metabolic consequences and possible etiology.
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Animal models with genetic or experimentally produced (lesions of hypothalamus) obesities are numerous and unlikely to ever be reduced to a single pathophysiologic entity. However, obese animals have many similar traits in common. They are all hyperinsulinemic, an abnormality that occurs early in
Hyperamylinemia, hyperinsulinemia, and insulin resistance in genetically obese LA/N-cp rats.
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The experimental evidence supporting a direct role for hyperinsulinemia as a cause of insulin resistance remains equivocal. Amylin, an islet beta-cell peptide cosecreted with insulin in response to nutrient stimuli, causes insulin resistance when infused into intact animals or applied to isolated
Obesity-independent hyperinsulinemia in nondiabetic first-degree relatives of individuals with type 2 diabetes.
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A close association between obesity and hyperinsulinemia is well recognized, but it is not known whether this relationship is affected by the genetic susceptibility to type 2 diabetes. Insulin response to a 75-g oral glucose load was evaluated in healthy nondiabetic Caucasians with first-degree
Serum leptin concentrations in hyperinsulinemia in the sets of obese, lipodystrophic and/or non-obese patients.
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OBJECTIVE
To study the relationship between serum leptin and circulating insulin under basal and in response to oral glucose administration in hyperinsulinemic patients with or without obesity.
METHODS
Fifteen female patients of known hyperinsulinemia provided material for the study. Leptin and
Leptin expression in hypothalamic PVN reverses dietary obesity and hyperinsulinemia but stimulates ghrelin.
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OBJECTIVE
In order to circumvent the multiple peripheral effects of hyperleptinemia and leptin resistance, the efficacy of leptin transgene expression in the hypothalamic paraventricular nucleus (PVN) to reinstate the central energy homeostasis in obesity was examined.
METHODS
A recombinant
Hemorheological aspects of the metabolic syndrome: markers of insulin resistance, obesity or hyperinsulinemia?
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The metabolic syndrome is a major health problem in western countries, due to the deleterious metabolic consequences of sedentarity and rich diet in the large part of the population who exhibits the so-called "thrifty phenotype". This syndrome, which is at high risk for diabetes and atherothrombosis
Relationship between beta-endorphin/beta-lipotropin, hyperglycemia, and hyperinsulinemia in obese male Zucker rats.
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The relationship between beta-endorphin(beta-EP)/beta-lipotropin(beta-LP) and insulin secretion in the basal state and after glucose challenge was studied in obese male Zucker rats and their lean littermates. Baseline plasma beta-EP/beta-LP concentrations were similar in the two groups of animals.
[Hyperinsulinism, heart rate variability and circadian variation of arterial pressure in obese hypertensive patients].
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OBJECTIVE
During insulin resistance, sympathetic nerve activity is increased. However insulin resistance is a common feature of obesity and essential hypertension, it is unclear if chronic hyperinsulinemia per se contributes to sympathetic overactivation. The purpose of our study was to explore++
Evidence for an association of high blood pressure and hyperinsulinemia in obese man.
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An association between hyperinsulinemia and hypertension has been suggested by epidemiological surveys. To assess whether this association is independent of the presence of other hyperinsulinemic states, such as obesity and glucose intolerance, we measured the insulin response to oral glucose in a
Temporal association between obesity and hyperinsulinemia in children, adolescents, and young adults: the Bogalusa Heart Study.
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Obesity is generally associated with hyperinsulinemia. However, whether obesity precedes or follows hyperinsulinemia is not clear. The present study examined the temporal nature of the association between obesity and hyperinsulinemia in a biracial (black-white) community-based population enrolled in
ENU mutagenesis identifies mice with morbid obesity and severe hyperinsulinemia caused by a novel mutation in leptin.
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BACKGROUND
Obesity is a multifactorial disease that arises from complex interactions between genetic predisposition and environmental factors. Leptin is central to the regulation of energy metabolism and control of body weight in mammals.
RESULTS
To better recapitulate the complexity of human
Hyperinsulinemia in the physiologic range is not superior to short-term fasting in suppressing insulin secretion in obese men.
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The negative-feedback control exerted by plasma insulin on beta-cell insulin release in normal-weight and obese subjects is still a matter of debate. Subjects submitted to a euglycemic insulin clamp undergo a suppression of insulin secretion that is due to both the infused insulin and the 2- to
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