Effect of pioglitazone on the fructose-induced abdominal adipose tissue dysfunction.

Aim. To test the potential role of PPARγ in the endocrine abdominal tissue dysfunction induced by feeding normal rats with a fructose rich diet (FRD) during three weeks. Methodology.

Islet NADPH oxidase activity is modulated unevenly by different secretagogues.

NADPH oxidase expression and activity have been measured in pancreatic islets under normal conditions, but its potential modulatory role upon insulin secretion remains unclear. We have currently studied NADPH oxidase activity in islets isolated from normal rats as well as the effect of its inhibition upon insulin secretion stimulated by different secretagogues. Glucose, arginine, fatty acids and KCl increased islet NADPH oxidase activity in a stimulus-dependent manner.

Early alterations in vascular contractility associated to changes in fatty acid composition and oxidative stress markers in perivascular adipose tissue.

Aim: To test the early effect of fructose-induced changes in fatty acid composition and oxidative stress markers in perivascular adipose tissue (PVAT) upon vascular contractility.

Methods: Adult male Wistar rats were fed a commercial diet without (CD) or with 10% fructose (FRD) in the drinking water for 3 weeks. We measured plasma metabolic parameters, lipid composition and oxidative stress markers in aortic PVAT.

Sitagliptin prevents the development of metabolic and hormonal disturbances, increased β-cell apoptosis and liver steatosis induced by a fructose-rich diet in normal rats.

The aim of the present study was to test the effect of sitagliptin and exendin-4 upon metabolic alterations, β-cell mass decrease and hepatic steatosis induced by F (fructose) in rats. Normal adult male Wistar rats received a standard commercial diet without (C) or with 10% (w/v) F in the drinking water (F) for 3 weeks; animals from each group were randomly divided into three subgroups: untreated (C and F) and simultaneously receiving either sitagliptin (CS and FS; 115.2 mg/day per rat) or exendin-4 (CE and FE; 0.

Glycoxidative stress-induced damage on lipid profile in a fructose-enriched diet model of insulin resistance in rats.

Objective: To study alterations in plasma lipid profile and oxidative damage to lipoprotein fractions (LF) and their fatty acids during an early insulin-resistant and increased oxidative state developed by a fructose-rich diet (FRD).

Methods And Results: Wistar rats were fed a commercial diet with (FRD) or without (CD) 10% fructose in the drinking water. After 3 weeks, plasma glucose, triglyceride (TG), insulin (I), fructosamine (F), free fatty acids (FFA) and lipid profile (total cholesterol [TC] and HDL-C, LDL-C and VLDL-C sub-fractions) were determined.

Fructose-rich diet-induced abdominal adipose tissue endocrine dysfunction in normal male rats.

We have currently studied the changes induced by administration of a fructose-rich diet (FRD) to normal rats in the mass and the endocrine function of abdominal (omental) adipose tissue (AAT). Rats were fed ad libitum a standard commercial chow and tap water, either alone (control diet, CD) or containing fructose (10%, w/vol) (FRD). Three weeks after treatment, circulating metabolic markers and leptin release from adipocytes of AAT were measured.

Abdominal adipose tissue: early metabolic dysfunction associated to insulin resistance and oxidative stress induced by an unbalanced diet.

The possible contribution of early changes in lipid composition, function, and antioxidant status of abdominal adipose tissue (AAT) induced by a fructose-rich diet (FRD) to the development of insulin resistance (IR) and oxidative stress (OS) was studied. Wistar rats were fed with a commercial diet with (FRD) or without 10% fructose in the drinking water for 3 weeks. The glucose (G), triglyceride (TG), and insulin (I) plasma levels, and the activity of antioxidant enzymes, lyposoluble antioxidants, total glutathione (GSH), lipid peroxidation as TBARS, fatty acid (FA) composition of AAT-TG as well as their release by incubated pieces of AAT were measured.

In vitro antagonism of Thielaviopsis paradoxa by Trichoderma longibrachiatum.

Seventy-nine Trichoderma strains were isolated from soil taken from 28 commercial plantations of Agave tequilana cv. 'Azul' in the State of Jalisco, Mexico. Nine of these isolates produced nonvolatile metabolites that completely inhibited the growth of Thielaviopsis paradoxa on potato dextrose agar plates.

Postprandial hyperglycemia and hyperlipidemia-generated glycoxidative stress: its contribution to the pathogenesis of diabetes complications.

Postprandial glucose and triglyceride increments after a mixed meal are more prolonged in people with type 1 and 2 diabetes or with impaired glucose tolerance than in normal individuals. Evidence in the literature suggests that these transient increases represent an additional and independent risk for chronic hyperglycemia to induce endothelial dysfunction, an important fact for the development of diabetic vascular complications. This article presents the more relevant mechanisms by which acute postprandial hyperglycemia and hyperlipidemia have been proved to determine the risk of reactive oxygen species overproduction, an increased synthesis of non enzymatic early-glycated and nitrated proteins, and a more atherogenic lipoprotein profile.

Serum carboxyl-terminal propeptide of procollagen type I in exercise-induced left ventricular hypertrophy.

Background: Left ventricular hypertrophy (LVH) induced by exercise is considered to be a physiologic adaptive mechanism without fibrogenic hyperactivity, as occurs in pathologic hypertrophy.

Hypothesis: This study investigated serum markers of collagen synthesis and echo parameters of left ventricular diastolic function (LVdf) in 22 male athletes.

Methods: Twenty-two highly competitive male athletes (10 cyclists, 12 soccer players) were studied with full history, clinical examination, Doppler echocardiogram, and serum concentration of the carboxyl-terminal propeptide of collagen type I (PIP).

Regression of hypertensive myocardial fibrosis by Na(+)/H(+) exchange inhibition.

We have recently reported that the inhibition of the Na(+)/H(+) exchanger (NHE) during 1 month in spontaneously hypertensive rats (SHR) is followed by regression of cardiomyocyte hypertrophy but not of myocardial fibrosis. The aim of this study was to evaluate whether a treatment of longer duration could reduce myocardial fibrosis and stiffness. SHR received 3.

Regression of cardiomyocyte hypertrophy in SHR following chronic inhibition of the Na(+)/H(+) exchanger.

Objective: Experiments were performed to examine the effect of chronic inhibition of the Na(+)/H(+) exchanger isoform-1 (NHE-1) on cardiac hypertrophy of spontaneously hypertensive rats (SHR).

Methods: SHR were orally treated during 1 month with two different doses (0.3 and 3.

[Lipoprotein glycation and glycoxidation: their importance in diabetes mellitus].

Chronic hyperglycemia induces an increase in the non enzymatic glycation of circulating and structural proteins together with a glucose-generated oxidative and carbonyl stress, known as glycoxidation. The physicochemical characteristics and the metabolism of lipoproteins are altered by glycation/glycoxidation and resemble those of other body proteins, except for the fact that there is a simultaneous glycoxidation of both protein and phospholipid components generating an oxidative stress that increases lipoxidation. Information gathered during the last few years suggests that, among lipoproteins, modified LDL would principally contribute to developing diabetic micro-macrovascular complications.

A useful model to study the effect of high sugar concentrations upon growth and enzymic activities of toad embryos and larvae.

The aim of this study was to develop an oviparous model suitable for studying the differential effects and mechanisms by which a high concentration of extracellular glucose and other sugars produce diabetes complications, particularly body growth retardation during development. Hence, we studied the experimental conditions necessary to obtain measurable effects of high sugar concentrations (5-mM glucose, mannitol, fructose and galactose) upon body growth and development of Bufo arenarum embryos and larvae, and upon the activity of aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and alkaline phosphatase (APP). Unfed animals kept in glucose showed lower body weight than controls at all stages, a condition only observed at stage 26 for animals kept in galactose and fructose.

Phytophthora cinnamomi as a Cause of Oak Mortality in the State of Colima, Mexico.

This research identifies the root pathogen Phytophthora cinnamomi as the primary cause of mortality in a 300-ha disease center of mixed oak trees in a native forest in southern Mexico. In increasing order of apparent field resistance to the disease, the major oak species are Quercus glaucoides, Q. peduncularis, and Q.

Early changes in the rat pancreatic B cell size induced by glucose.

The perimeter, cell area and volume density (Vvi) of B cells and exocytotic images present in these cells were measured in rat pancreas perfused with 3.3 or 16.6 mM glucose.

Effect of extracellular alkalosis upon calcium distribution within the B cells.

Insulin secretion and the pattern of calcium distribution in B cells, assessed with the pyroantimonate precipitation technique, were simultaneously studied in rat pancreases perfused with 3.3 and 16.6 mM glucose solutions of pH 7.

Effect of verapamil and trifluoperazine upon glucose-induced calcium distribution within B cells.

Insulin secretion and B-cell calcium distribution, assessed with the pyroantimonate precipitation technique, were studied in rat pancreases perfused with glucose (3.3 or 16.6 mM) alone or together with verapamil or trifluoperazine (TFP).

Quantitative ultrastructural changes induced by glucose in pancreatic B cells.

The acute ultrastructural changes induced by glucose upon the B cells were studied in normal rat pancreas perfused with 3.3 and 16.6 mmol/l glucose.

Glucagon secretion and intracellular calcium distribution in pancreatic A cells.

Quantitative changes in the distribution of intracellular calcium in A cells from perfused rat pancreas in relation to the secretory state of A cells were studied with the pyroantimonate technique for calcium precipitation. A cells stimulated with a 3.3 mM glucose concentration in the perfusate presented numerous calcium precipitates attached to cell membranes, nucleus, cytoplasm and secretion granules.

Ultracytochemical nuclear calcium distribution in pancreatic B cells: its relation to glucose-stimulated insulin secretion.

Calcium distribution in pancreatic B cells was studied, with the aid of the pyroantimonate technique, at different times of glucose-induced secretory activity in the perfused rat pancreas. Specificity of the pyroantimonate precipitates for calcium was assessed by EGTA cross-incubation. Quantitative studies for these calcium pyroantimonate precipitates were performed by a morphometric technique.

Chronobiological aspects of blood glucose regulation: a new scope for the study of diabetes mellitus.

The levels of blood glucose undergo circadian variations in every species studied. Such rhythm is the consequence of the oscillation in the rate of provision and consumption of glucose. The liver plays an important role in this rhythm, retaining or releasing glucose from or to the circulation.

Sequential determination of calcium distribution in B cells at the various phases of glucose-induced insulin secretion.

Localization and quantification of calcium pyroantimonate precipitates within the B cells, and determination of insulin secretion were performed in rat pancreas perfused with 3.3 and 16.6 mmol/l glucose.

Glucagon and insulin secretion during acid-base alterations.

Previously, we reported that change from the normal pH of 7.4 surrounding the islet cells to 7.8 results in a decreased B-cell response to 16.