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1.
The effects of prolonged substitution of readily digested carbohydrates (wheat starch) for poorly digested carbohydrates (mixture of various fibres and crude potato starch) on plasma lipids, lipoproteins and hormones were investigated in Zucker, genetically obese rats. Lean rats were also studied in parallel. Usually, plasma lipid and insulin levels and insulin/glucose ratio were higher in obese rats vs. their lean littermates. High-fibre diet intake led to weight loss in both obese and lean rats. With a high-fibre diet, plasma lipid, insulin and glucose postprandial levels in both groups were reduced when compared with their respective control animals. Dietary fibre modified the lipoprotein profile. Triglycerides and cholesterol were reduced in all studied lipoprotein fractions. The study of high density lipoprotein (HDL) fraction in rats fed a high-fibre diet demonstrated a decrease in the HDL1 subpopulation and in the apolipoprotein (apo)E proportion. The findings show that a high-fibre diet modulates plasma lipid, insulin and glucose levels and modifies the plasma lipoprotein distribution and composition in normolipaemic, lean rats as well as in hyperlipaemic, genetically obese rats.  相似文献   

2.
The genetically obese Zucker rat (fa/fa) is characterized by a severe resistance to the action of insulin to stimulate skeletal muscle glucose transport. The goal of the present study was to identify whether the defect associated with this insulin resistance involves an alteration of transporter translocation and/or transporter activity. Various components of the muscle glucose transport system were investigated in plasma membranes isolated from basal or maximally insulin-treated skeletal muscle of lean and obese Zucker rats. Measurements of D- and L-glucose uptake by membrane vesicles under equilibrium exchange conditions indicated that insulin treatment resulted in a four-fold increase in the Vmax for carrier-mediated transport for lean animals [from 4.5 to 17.5 nmol/(mg.s)] but only a 2.5-fold increase for obese rats [from 3.6 to 9.1 nmol/(mg.s)]. In the lean animals, this increase in glucose transport function was associated with a 1.8-fold increase in the transporter number as indicated by cytochalasin B binding, a 1.4-fold increase in plasma membrane GLUT4 protein, and a doubling of the average carrier turnover number (intrinsic activity). In the obese animals, there was no change in plasma membrane transporter number measured by cytochalasin B binding, or in GLUT4 or GLUT1 protein. However, there was an increase in carrier turnover number similar to that seen in the lean litter mates. Measurements of GLUT4 mRNA in red gastrocnemius muscle showed no difference between lean and obese rats. We conclude that the insulin resistance of the obese rats involves the failure of translocation of transporters, while the action of insulin to increase the average carrier turnover number is normal.  相似文献   

3.
Summary. The levels of plasma insulin and C-peptide during exercise and subsequent recovery have been determined in obese non-diabetics, obese diabetics Type II and middle-aged female controls. It has been found that exercise reduces levels of peptides both in the control and in the obese non-diabetic group. This effect of acute exercise was found blunted in the obese diabetic group. Non-diabetic obese subjects pretreated with phentolamine showed no reduction either in plasma insulin or C-peptide levels during exercise. During the recovery, the level of plasma insulin returned promptly to the pre-exercise value in the control group but increased above the resting value in obese subjects, both non-diabetic and diabetic. In controls and non-diabetic obeses the increment of C-peptide: insulin molar ratio occurred early after the onset of exercise and then returned to the resting value despite the exercise being continued. The plasma C-peptide:insulin molar ratios were reduced during the first 15 min of recovery period in obese non-diabetic subjects and returned to normal in the next 15 min. The latter may suggest that reduced insulin removal could also contribute to the increase in plasma insulin values in the obeses during recovery.  相似文献   

4.
The present study tested the hypothesis that altered vascular regulation of arachidonic acid enzymes in obese Zucker rats contributes to renal damage. Protein expression of CYP450 (cytochrome P450) and COX (cyclo-oxygenase) enzymes in renal microvessels was studied in obese and lean Zucker rats at 20-21 weeks of age. Body weight and blood glucose averaged 649+/-13 g and 142+/-10 mg/dl in obese Zucker rats compared with 437+/-10 g and 111+/-5 mg/dl in age-matched lean Zucker rats. Renal microvascular CYP4A and COX-2 protein levels were increased and CYP2C protein levels decreased in obese Zucker rats. TX (thromboxane) B2 excretion was 2-fold higher and PG (prostaglandin) E2 excretion significantly lower in obese Zucker rats. Additional studies investigated the ability of the COX-2 inhibitor, rofecoxib, to slow the progression of renal injury in obese Zucker rats. Rofecoxib treatment decreased urinary PGF2alpha and 8-isoprostane levels in obese Zucker rats. Renal microvessel mRNA expression of pro-inflammatory chemokines was decreased in COX-2-inhibitor-treated obese Zucker rats. Urinary albumin excretion, an index of kidney damage, averaged 95+/-11 mg/day in vehicle-treated and 9+/-1 mg/day in rofecoxib-treated obese Zucker rats. Glomerulosclerosis, characterized by mesangial expansion, tubulo-interstitial fibrosis and extracellular matrix accumulation, was prominent in obese Zucker rats compared with a lack of damage in age-matched lean Zucker rats and rofecoxib-treated obese Zucker rats. These results suggest that altered vascular arachidonic acid enzymes contribute to the renal damage, and that COX-2 inhibition decreases glomerular injury in obese Zucker rats.  相似文献   

5.
Many digestive complaints are associated with abnormalities in gastrointestinal peptide hormone function. To investigate the effect of obesity on the release of pancreatic peptide hormones, we have compared the release of insulin and glucagon in non-obese-obese Dutch women in response to isocaloric mixed meals and to Naloxone, an opioid antagonist. Healthy premenopausal women who were separated into three groups based on body mass index (BMI less than 23; 23-27, greater than 28), were fed 600-calorie breakfasts. Higher fasting levels of plasma insulin and glucagon occurred in obese (BMI greater than 28) than lean (BMI less than 23) women, while glucagon and insulin release after a high fat meal occurred in obese women. Naloxone administration in obese women decreased plasma insulin and glucagon, but in lean women, naloxone increased plasma glucagon but did not alter plasma insulin levels. Results indicate differences in opiate effects on pancreatic function in non-obese-obese women.  相似文献   

6.
Both insulin resistance and hyperinsulinemia have been reported to be independent risk factors for cardiovascular diseases. However, little is known regarding insulin signaling in the vascular tissues in insulin-resistant states. In this report, insulin signaling on the phosphatidylinositol 3-kinase (PI 3-kinase) and mitogen-activated protein (MAP) kinase pathways were compared in vascular tissues of lean and obese Zucker (fa/fa) rats in both ex vivo and in vivo studies. Ex vivo, insulin-stimulated tyrosine phosphorylation of insulin receptor beta subunits (IRbeta) in the aorta and microvessels of obese rats was significantly decreased compared with lean rats, although the protein levels of IRbeta in the 2 groups were not different. Insulin-induced tyrosine phosphorylation of insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) and their protein levels were decreased in the aorta of obese rats compared with lean rats. The association of p85 subunit to the IRS proteins and the IRS-associated PI 3-kinase activities stimulated by insulin in the aorta of obese rats were significantly decreased compared with the lean rats. In addition, insulin-stimulated serine phosphorylation of Akt, a downstream kinase of PI 3-kinase pathway, was also reduced significantly in isolated microvessels from obese rats compared with the lean rats. In euglycemic clamp studies, insulin infusion greatly increased tyrosine phosphorylation of IRbeta- and IRS-2-associated PI 3-kinase activity in the aorta of lean rats, but only slight increases were observed in obese rats. In contrast, insulin stimulated tyrosine phosphorylation of MAP kinase (ERK-1/2) equally in isolated microvessels of lean and obese rats, although basal tyrosine phosphorylation of ERK-1/2 was higher in the obese rats. To our knowledge, these data provided the first direct measurements of insulin signaling in the vascular tissues, and documented a selective resistance to PI 3-kinase (but not to MAP kinase pathway) in the vascular tissues of obese Zucker rats.  相似文献   

7.
Some combinations of antihypertensive agents were shown to reduce proteinuria in patients with renal failure. However, preventive effects of such combinations on renal structure and function are presently unknown when treatment is administered before the onset of renal abnormalities. We thus investigated the long-term effects of an angiotensin-converting enzyme (ACE) inhibitor (perindopril)/diuretic (indapamide) combination (per/ind) in the Zucker rat, a classical model of chronic renal failure associated with obesity, hyperlipidemia, and insulin resistance. Two-month-old lean and obese Zucker rats, presenting normal renal structure and function at this young age, received per/ind (0.76 + 0.24 mg/kg of body weight/day) or the vehicle of this combination by daily gavage. After 8.5 consecutive months of treatment, those 10.5-month-old rats were used for determination of renal structural and functional parameters which were examined using standard renal clearance experiments and kidney tissue analysis. Per/ind prevented focal and segmental glomerular hyalinosis and tubulo-interstitial damage in obese rats. Treatment was also associated with a significant reduction in several staining markers of glomerular and interstitial fibrosis. The hypertrophy of superficial glomeruli and the mesangial expansion of deep glomeruli observed in control rats were reduced in per/ind-treated obese rats. The severe proteinuria observed in 10.5-month-old control obese rats was prevented by per/ind, while glomerular filtration and renal hemodynamic parameters reached similar values to those obtained in lean animals. These results show that long-term treatment with this ACE inhibitor/diuretic combination protects renal structure and function in the obese Zucker rat, emphasizing the potential efficiency of such therapy in renal failure prevention.  相似文献   

8.
As in women receiving oestrogens the administration of 17beta-oestradiol to ovariectomized female rats caused a rise in fasting plasma triglycerides and a fall in plasma glucose. Progesterone, on the other hand, had no significant effects. In the oestradiol treated rats, the portal vein basal insulin levels were slightly reduced. Oestradiol, however, had a marked suppressive effect on the alpha cells of the pancreas resulting in a greater reduction in basal glucagon and impaired glucagon response to alanine infusions. The relative insulin to glucagon (I/G) molar concentration ratio in portal vein blood was increased. Oestradiol also produced a dose dependent increase in the activity of the liver lipogenic enzymes, acetyl CoA carboxylase and fatty acid synthetase. On the other hand, the activity of the gluconeogenic rate limiting enzyme phosphoenol-pyruvate carboxykinase (PEPCK) was inhibited. The cross-over pattern of gluconeogenic intermediates confirmed inhibition of gluconeogenesis at this step, an effect which is similar to that induced by relative insulin 'excess'. Progesterone produced an increase in the portal vein insulin concentrations. Both the basal and the alanine-stimulated glucagon levels were also increased. The I/G molar ratio in portal vein blood of progesterone treated rats remained unaltered and the hepatic lipogenic and gluconeogenic enzyme activities were similar to control animals. These data suggest that insulin activity is increased relative to glucagon in the liver of oestradiol-treated rats due to the rise in portal vein I/G ratio. The changes in liver lipogenic and gluconeogenic enzymes and the alterations in fasting plasma triglycerides and glucose in response to oestrogens could be secondary to this effect.  相似文献   

9.
The effect of glucagon (50 ng/kg/min) on arterial glycerol concentration and net splanchnic production of total ketones and glucose was studied after an overnight fast in four normal and five insulin-dependent diabetic men. Brachial artery and hepatic vein catheters were inserted and splanchnic blood flow determined using indocyanine green. The glucagon infusion resulted in a mean circulating plasma level of 4,420 pg/ml.In the normal subjects, the glucagon infusion resulted in stimulation of insulin secretion indicated by rising levels of immunoreactive insulin and C-peptide immunoreactivity. Arterial glycerol concentration (an index of lipolysis) declined markedly and net splanchnic total ketone production was virtually abolished. In contrast, the diabetic subjects secreted no insulin (no rise in C-peptide immunoreactivity) in response to glucagon. Arterial glycerol and net splanchnic total ketone production in these subjects rose significantly (P=<0.05) when compared with the results in four diabetics who received a saline infusion after undergoing the same catheterization procedure.Net splanchnic glucose production rose markedly during glucagon stimulation in the normals and diabetics despite the marked rise in insulin in the normals. Thus, the same level of circulating insulin which markedly suppressed lipolysis and ketogenesis in the normals failed to inhibit the glucagon-mediated increase in net splanchnic glucose production.It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release.  相似文献   

10.
Diabetic patients have a decreased incidence of acute respiratory distress syndrome, but the mechanism responsible for the decreased incidence is uncertain. Reabsorption of alveolar edema fluid (alveolar fluid clearance) has been considered to play an important role in resolution of acute respiratory distress syndrome. However, little is known regarding alveolar fluid clearance in diabetes mellitus. Since the obese Zucker rat has been used as an experimental model for diabetes mellitus, we determined if alveolar fluid clearance increased in the obese Zucker rat. First, we compared alveolar fluid clearance in obese Zucker rats with that in lean Zucker rats and Sprague-Dawley (SD) rats. Then, we determined the role of sodium channel, Na,K-ATPase, and beta(2)-adrenoceptor, which drives alveolar fluid clearance, in obese Zucker rats. Alveolar fluid clearance was estimated by the progressive increase in alveolar albumin concentrations in the isolated lungs. We found that basal alveolar fluid clearance in obese Zucker rats was two-fold greater than that in lean Zucker rats and SD rats. The mRNA expression of alpha(1)-, beta(1)-Na, K-ATPase and beta(2)-adrenoceptor, but not mRNA expression of sodium channel, increased in obese Zucker rats. A selective beta(2)-agrenergic antagonist, but not a Na, K-ATPase inhibitor, specifically inhibited the increase in alveolar fluid clearance in obese Zucker rats. These results indicate that overexpression of beta(2)-adrenoceptor primarily increases basal alveolar fluid clearance in the obese Zucker rat. We speculate that the stimulation of alveolar fluid clearance ameliorates acute respiratory distress syndrome in patients with diabetes mellitus.  相似文献   

11.
The etiology of the alterations in calcitonin (CT) secretion and plasma calcium of genetically obese (fa/fa) rats is unknown. In this study, we tested the postulate that there is an early occurrence of abnormalities in CT biosynthesis by thyroid glands of these rodents. Male genetically obese Zucker (fa/fa) rats and their lean littermates were therefore studied from 30 days to 10 months of age. Obese animals were characterized by hypercalcemia (delta approximately equal to 1 mg/dl), already present at 30 days of age. Increased thyroidal CT stores began at 6 weeks of age in fatty rats. Plasma CT levels were decreased in obese animals from 30 days to 10 weeks of age and were not different in leans and fatties 2 weeks later, but were higher at 10 months in fatty rats. Poly A + RNA were extracted from thyroid glands and subjected to translation assays. After SDS-PAGE, specific immunoprecipitates were autoradiographed and quantified by integration. A similar translation product with an apparent mol wt of 15,000 was specifically immunoprecipitated with CT antisera in obese (fa/fa) and lean Zucker rats at different ages. In 30-day-old fatty rats, a 50% decrease in translatable CT mRNA was observed in association with decreased plasma CT levels. In 12-week-old fatty rats, the translatable CT mRNA activity was unchanged or higher when compared to lean littermates, and clearly higher in 10-month-old fatty rats. The CT mRNA levels measured by dot-blot or northern blot hybridization paralleled at each stage studied the CT mRNA activity, determined by translation. It was concluded that in basal conditions, plasma CT level variations during development reflect the biosynthetic activity of C cells in genetically obese rats. The data presented in this study strengthen the point of an early occurrence of abnormalities in CT mRNA activity and in plasma calcium of fa/fa rats.  相似文献   

12.
In vivo and in vitro alterations in drug metabolism and the extent of enzyme induction of the hepatic microsomal cytochrome P-450 system were evaluated in obese and lean Zucker and lean Sprague-Dawley rats. Phenobarbital enzyme-inducing regimens were administered p.o. to achieve similar steady-state phenobarbital plasma concentrations. Control rats received p.o. placebo solution. No significant intra- or inter-strain differences in antipyrine clearance (milliliters per hour) or apparent volume of distribution (liters) were observed between the placebo-treated lean Sprague-Dawley, lean Zucker and obese Zucker rats. Intra- and inter-strain differences in hepatic microsomal protein and cytochrome P-450 content were observed. Compared to placebo, antipyrine clearance (milliliters per hour) after chronic phenobarbital pretreatment was increased in the Sprague-Dawley (198%) and lean Zucker rats (131%), but not significantly altered in the obese Zucker rats. Similarly, increases in hepatic weight, whole liver microsomal protein and cytochrome P-450 content were also observed in the Sprague-Dawley (34, 124 and 352%, respectively) and the lean Zucker rats (24, 96 and 249%, respectively). However, no significant alterations in these parameters were observed in the obese Zucker rats after phenobarbital treatment. Results from these in vivo and in vitro studies implicate alterations in drug metabolism and genetic differences in cytochrome P-450 content in Zucker rats relative to the Sprague-Dawley strain. Obese Zucker rats failed to exhibit a significant induction response after phenobarbital pretreatment.  相似文献   

13.
The present study evaluated the involvement of glucose transport and phosphorylation in glucose-stimulated insulin release from pancreatic islets. Using quantitative histochemical techniques, we investigated basal islet glucose content, islet glucose uptake in situ during acute extreme experimental hyperglycemia, and islet glucokinase activity in several animal models of diabetes and obesity. The basal islet glucose content in anaesthetized diabetic or obese rodents was either the same or higher than that in their relevant controls. The rate of glucose uptake of islet tissue in these animals after an i.v. glucose injection was different. The db+/db+ mouse and the obese Zucker rat exhibited significantly reduced islet glucose uptake rates. RIP-cHras transgenic mice, BHE/cdb rats and partially pancreatectomized rats showed normal islet glucose uptake rates. The activity of islet glucokinase was increased to a different degree related to the blood glucose level. All five animal models of diabetes or obesity exhibited either a delay or a reduction of insulin release in response to supra maximal glucose stimulation. Our results indicate that the impairment of glucose-induced insulin release in diabetes is not consistently associated with a reduction of islet glucose uptake nor a change of glucokinase activity.  相似文献   

14.
Role of nitric oxide in obesity-induced beta cell disease.   总被引:7,自引:3,他引:7       下载免费PDF全文
Here we report that free fatty acid-induced suppression of insulin output in prediabetic Zucker diabetic fatty (ZDF) rats is mediated by NO. When normal islets were cultured in 2 mM FFA, NO production and basal insulin secretion increased slightly. In cultured prediabetic ZDF islets, FFA induced a fourfold greater rise in NO, upregulated mRNA of inducible nitric oxide synthase (iNOS), and reduced insulin output; both nicotinamide and aminoguanidine, which lower NO, prevented the FFA-mediated increase in iNOS mRNA, reduced NO, and minimized the loss of insulin secretion. In vivo nicotinamide or aminoguanidine treatment of prediabetic ZDF rats prevented the iNOS expression in islets and decreased beta cell dysfunction while blocking beta cell destruction and hyperglycemia. We conclude that NO-lowering agents prevent adipogenic diabetes in obese rats.  相似文献   

15.
Effects of genetic obesity on renal structure and function in the Zucker rat   总被引:10,自引:0,他引:10  
Although hyperphagia and obesity in the Zucker rat strain have been reported to be associated with spontaneous focal glomerulosclerosis (FGS), little is known about the age of onset and the natural history of hypertension, albuminuria, renal function, and glomerular injury in this model. We systematically investigated renal structure and function in obese male Zucker rats. Lean male littermates were used as controls. Obese rats developed glomerular mesangial matrix expansion and albuminuria by 14 weeks of age. These changes occurred despite normal inulin clearance (2.2 +/- 0.6 ml/min obese vs. 2.0 +/- 0.4 ml/min lean, P greater than 0.1) and filtration fraction (0.32 +/- 0.08 obese vs. 0.34 +/- 0.06 lean, P greater than 0.1), suggesting that increased glomerular filtration and renal plasma flow were not a prerequisite for the development of FGS. By 28 weeks of age, FGS was evident in seven of eight obese rats, and at 68 weeks of age all obese rats had marked FGS. Mean systolic blood pressure was elevated by 11 to 25 mm Hg in obese rats at all ages. Although the pathogenesis of glomerular injury is unknown, our data demonstrate that microalbuminuria, mild hypertension, and mesangial matrix expansion precede the development of progressive FGS in obese Zucker rats.  相似文献   

16.
Marked diuresis has previously been reported after administration of kappa opioid agonists. The present study shows that this effect is stereospecific; MR-2034 markedly increased urinary output over the dose range 0.08 to 1.25 mg/kg, whereas the opposite isomer, MR-2035, was markedly less potent. Bremazocine increased urinary output in Long-Evans hooded and Sprague-Dawley albino rats as well as lean and fatty Zucker rats. In the lean Zucker and the albino rats, bremazocine produced an inverted U-shaped diuretic dose-effect curve, an effect characteristic of kappa agonists with mu agonist activity. This pattern was not seen with the fatty Zucker rats or the Long-Evans hooded rats. The full kappa agonists bremazocine, ethylketazocine and U-50,488 increased urinary output under three different conditions of hydration: water loaded, normal hydration and water deprived. In contrast, the partial kappa agonists reliably only increase urinary output under the normal hydration condition. The diuretic effects of full and partial kappa agonists correlated with plasma vasopressin levels in water-deprived rats. The full kappa agonists (ethylketazocine, U-50,488, tifluadom and MR-2034) suppressed plasma vasopressin levels below the threshold of detectability of the radioimmunoassay, whereas the partial kappa agonists (nalorphine and butorphanol) suppressed vasopressin levels compared with control values but did not have the efficacy of the full kappa agonists. All these results support the hypothesis that kappa agonists produce their diuretic effect by suppression of plasma vasopressin levels.  相似文献   

17.
Heterotopic pancreas transplantation in type I diabetic patients does not correct hyperglucagonemia, which is thought to be due to insufficiently suppressed glucagon release by the host pancreas. The diabetogenic effects of glucagon then have to be corrected by higher than normal insulin secretion from the transplant, with the attendant risk of earlier loss of islet cell function, and development of atherosclerosis. To establish whether this situation can be prevented, we investigated glucose homeostasis and blood lipids, as well as fecal fat and chymotrypsin as indicators for pancreatic exocrine function 14 weeks after orthotopic pancreas transplantation in inbred rats. The pancreas was resected before orthotopic transplantation of the donor pancreas with portal venous drainage (n=8). Laparotomized animals served as controls (n=8). Basal plasma glucagon, basal plasma insulin to glucagon molar ratio, and basal and integrated incremental responses of plasma glucose, insulin, and C-peptide after an oral glucose load (2 g/kg body weight) were similar in both groups. However, hepatic insulin clearance was slightly but significantly lower in the transplanted group (1.1± 0.1 vs 1.6±0.2; P<0.05). Basal plasma levels of free fatty acids, phospholipids, triglycerides, cholesterol, low-density lipoproteins, and high-density lipoproteins were unchanged after transplantation. Also unchanged were fecal fat and chymotrypsin levels, thus indicating preserved pancreatic exocrine function. We concluded that orthotopic pancreas transplantation with portal venous drainage achieves almost optimal metabolic control with respect to endocrine and exocrine pancreatic function as well as blood lipids. This technique could therefore be used to treat combined endocrine and exocrine  相似文献   

18.
Hypothalamic regulatory peptides in obese and lean Zucker rats.   总被引:1,自引:0,他引:1  
1. Hypothalamic concentrations of nine peptides with experimental effects on energy balance were compared in obese (fa/fa) and lean (Fa/?) male Zucker rats. To determine whether any peptide differences between obese and lean rats might be due to the overweight condition per se, separate groups of obese rats were food-restricted to reduce their body weight to lean values. 2. Concentrations of neuromedin B, a bombesin-like peptide, in the central hypothalamus were significantly higher in obese than in lean rats. This difference was not affected in food-restricted obese rats. 3. Hypothalamic levels of neuropeptide Y, an extremely potent central appetite stimulant, were similar in lean and freely fed obese rats but central hypothalamic levels of neuropeptide Y rose significantly in food-restricted obese rats. 4. These findings suggest that disturbances in hypothalamic neuromedin B concentrations may be involved in the obesity syndrome of the fa/fa Zucker rat. Increased central hypothalamic levels of neuropeptide Y in food-restricted rats suggest that this peptide may help to defend body weight by stimulating eating after weight loss.  相似文献   

19.
BACKGROUND: Childhood obesity is associated with lower plasma levels of lipophilic antioxidants which may contribute to a deficient protection of low-density lipoproteins (LDL). An increased plasma level of oxidized LDL in obese people with insulin resistance has been demonstrated. The lipophilic antioxidant coenzyme Q10 (CoQ10) is known as an effective inhibitor of oxidative damage in LDL as well. The aim of the present study was to compare the CoQ10 levels in obese and normal weight children. METHODS: The CoQ10 plasma concentrations were measured in 67 obese children (BMI>97th percentile) and related to their degree of insulin resistance. Homeostasis model assessment (HOMA) was used to detect the degree of insulin resistance. The results were compared to a control group of 50 normal weight and apparently healthy children. The results of the CoQ10 levels were related to the plasma cholesterol concentrations. RESULTS: After adjustment to plasma cholesterol, no significant difference in the CoQ10 levels between obese and normal weight children could be demonstrated. Furthermore, there was no difference between insulin-resistant and non-insulin-resistant obese children. CONCLUSION: CoQ10 plasma levels are not reduced in obese children and are not related to insulin resistance.  相似文献   

20.
Gliquidone (a second generation sulphonylurea) was administered orally to normal rats 1 h before killing. Gliquidone treatment led to a decrease in plasma glucose, an increase in insulin and a diminution in glucagon concentration. Insulin binding to liver plasma membranes was enhanced by 40% in comparison with controls, whereas glucagon binding was slightly diminished. These findings indicate a greater sensitivity of liver cells to insulin during sulphonylurea treatment and support the view that sulphonylureas potentiate insulin action on the liver.  相似文献   

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