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hyperinsulinism/albumin
Veza se sprema u međuspremnik
Page 1 od 114 rezultati
Albumin synthesis rates are not responsive to hyperglycemic hyperinsulinemia in postoperative patients.
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BACKGROUND
Insulin regulates albumin synthesis in vitro and in various experimental models. The current study was undertaken to determine the effects of a physiologic hyperinsulinemia on albumin synthesis in postoperative patients in whom plasma albumin concentrations are decreased.
METHODS
Studies
Role of salt sensitivity, blood pressure, and hyperinsulinemia in determining high upper normal levels of urinary albumin excretion in a healthy adult population.
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BACKGROUND
The objective of this study was to investigate the role of blood pressure (BP), salt sensitivity (SS), and the cardiovascular metabolic syndrome in determining the urinary albumin excretion (UAE) in glucose-tolerant, normoalbuminuric (<20 mg/day) healthy adults.
RESULTS
We evaluated 177
Increased transcapillary escape rate of albumin in nondiabetic men in response to hyperinsulinemia.
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Diabetic patients manifest increased vascular permeability. To determine whether insulin per se might increase vascular permeability, five nondiabetic men were studied by the hyperinsulinemic-euglycemic clamp technique. Each subject received a 0.72-nmol/kg body wt i.v. insulin bolus, followed by a
Relationship between urinary albumin excretion, body composition, and hyperinsulinemia in normotensive glucose-tolerant adults.
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OBJECTIVE
Elevated urinary albumin excretion (UAE) has been associated with insulin resistance and is suggested to be elevated in prediabetic individuals. Upper body obesity, especially visceral obesity, predicts insulin resistance and development of type 2 diabetes. We examined whether UAE clusters
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
Microalbuminuria in never-treated hypertensives: lack of relationship to hyperinsulinemia and genetic predisposition to hypertension.
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We evaluated the relationship of microalbuminuria to hyperinsulinemia and family history of hypertension in 92 never-treated essential hypertensives (mean 24-h blood pressure >140 or 90 mm Hg), with positive (F+) or negative (F-) family history of hypertension: 31 had microalbuminuria (MA+) (urinary
Synergistic proliferation induced by insulin and glycated serum albumin in rat vascular smooth muscle cells.
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Hyperglycemia, advanced glycation end products (AGEs), hyperinsulinemia and dyslipidemia may play roles in the development of diabetes-associated atherosclerosis and post-angioplasty restenosis. Clinically, their effects seem to be synergic. However, few studies have focused on the synergistic
Predictors of urinary albumin excretion in women with polycystic ovary syndrome.
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OBJECTIVE
To evaluate urinary albumin excretion (UAE) in normotensive and nondiabetic women with polycystic ovary syndrome (PCOS) in relation to their clinical, endocrine, and metabolic profiles.
METHODS
Observational study.
METHODS
University fertility center.
METHODS
Sixty-three women with PCOS
Elevated albumin excretion in nonmodulating essential hypertensive patients.
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Nonmodulating (NM) essential hypertensives are characterized by abnormal renal and aldosterone responses to angiotensin II. Recently, hyperinsulinemia, hypercholesterolemia, and an increased prevalence of family history of hypertension and myocardial infarction have been shown in NM hypertensives.
Insulin alters nuclear factor-lambdaB and peroxisome proliferator-activated receptor-gamma protein expression induced by glycated bovine serum albumin in vascular smooth-muscle cells.
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In both type 2 diabetes and insulin-resistance syndromes, hyperglycemia and advanced glycation end products (AGEs) activate the transcription factor nuclear factor-kappaB (NF-kappaB) through a mechanism that partly involves the generation of reactive oxygen species (ROS). The contribution of
Dyslipidemia and hyperinsulinemia in children and adolescents with chronic liver disease: relation to disease severity.
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BACKGROUND
Lipid metabolism is profoundly disturbed in chronic liver diseases (CLD). Moreover, patients with cirrhosis displayed chronically elevated serum insulin (SI) concentrations.
OBJECTIVE
The aim of this work was to assess fasting lipid profile (FLP) and SI levels among Egyptian patients with
A novel factor for primary arteriovenous fistula failure: hyperinsulinism.
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BACKGROUND
Dysfunction of vascular access is an important reason of morbidity for dialysis patients and it is a major factor affecting the economical burden of hemodialysis. The preferred type of vascular access is creation of an arteriovenous fistula (AVF). However, the problem of fistula
Glycation does not modify bovine serum albumin (BSA)-induced reduction of rat aortic relaxation: the response to glycated and nonglycated BSA is lost in metabolic syndrome.
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The effects of nonglycated bovine serum albumin (BSA) and advanced glycosylation end products of BSA (AGE-BSA) on vascular responses of control and metabolic syndrome (MS) rats characterized by hypertriglyceridemia, hypertension, hyperinsulinemia, and insulin resistance were studied. Albumin and in
Dietary supplementation with alpha-amylase inhibitor wheat albumin to high-fat diet-induced insulin-resistant rats is associated with increased expression of genes related to fatty acid synthesis in adipose tissue.
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It is well-known that insulin resistance induces lipid abnormalities by decreasing insulin actions in adipose tissue. This study examined the effects of inhibiting postprandial hyperglycemia/hyperinsulinemia, using the alpha-amylase inhibitor wheat albumin (WA), on the expression of genes related to
Hyperinsulinemia, circadian variation of blood pressure and end-organ damage in hypertension.
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BACKGROUND
Some patients with essential hypertension display hyperinsulinemia and/or insulin resistance. A relationship between hyperinsulinemia and blood pressure has not been conclusively established. Some evidence points to a relationship between hyperinsulinemia and evidence of cardiovascular
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