Biochemical and Molecular Roles of nutrients A Fructose-Rich Diet Decreases Insulin-Stimulated Glucose Incorporation into Lipids but Not Glucose Transport in Adipocytes of Normal and Diabetic Rats1 (original) (raw)
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Fructose-induced in vivo insulin resistance and elevated plasma triglyceride levels in rats
The American journal of clinical nutrition, 1989
Insulin action was assessed by using the hyperinsulinemic (approximately 800 pmol/L) euglycemic clamp in rats fed equal amounts of glucose or fructose (35% of calories) for 4 wk. The glucose infusion rate required to maintain euglycemia was decreased in fructose-fed animals (14.6 +/- 1.4 vs 21.8 +/- 1.1 for glucose-fed rats, p less than 0.001) with this whole-body effect contributed to equally by an impairment in hepatic insulin action and a reduction in peripheral glucose disposal in a range of tissues. There was no difference in basal glucose turnover, energy expenditure, or postprandial blood glucose and insulin responses to the diets. In the fructose-fed rats there was an increase in fasting triglyceride levels by 2 wk. Euglycemic clamp glucose disposal correlated positively and clamp hepatic glucose output correlated negatively with fasting triglyceride levels. In summary, fructose but not glucose feeding led to impaired insulin action in both the liver and peripheral tissues, ...
Journal of Nutrition
Because we found previously that fructose feeding could alter lipolytic responses to isoproterenol and insulin in normal rats, we studied the effects of the same diet in neonatal, streptozotocin-diabetic rats. Twenty-seven 5-wk-old diabetic Sprague-Dawley rats were fed a diet containing 57% carbohydrate as either fructose, dextrose or starch for 6 wk. At the end of the nutritional period, plasma glucose and insulin concentrations in fed rats were similar in the three diabetic groups. Plasma triacylglycerol concentrations were higher in the fructose-fed group than in the other two groups (P < 0.05). Neither the maximal adipocyte lipolytic response (fructose = 1147 +/- 165%, starch = 1823 +/- 329% and dextrose = 1287 +/- 239% of basal values) nor the sensitivity to isoproterenol (ED50) was changed by the dietary carbohydrate exchange. The maximal antilipolytic action of insulin (starch = 68 +/- 10%, dextrose = 41 +/- 13%, fructose = 95 +/- 29% of stimulated lipolysis values) was co...
Metabolic syndrome signs in Wistar rats submitted to different high-fructose ingestion protocols
British Journal of Nutrition, 2009
In search of an adequate model for the human metabolic syndrome, the metabolic characteristics of Wistar rats were analysed after being submitted to different protocols of high fructose ingestion. First, two adult rat groups (aged 90 d) were studied: a control group (C1; n 6) received regular rodent chow (Labina, Purina) and a fructose group (F1; n 6) was fed on regular rodent chow. Fructose was administered as a 10 % solution in drinking water. Second, two adult rat groups (aged 90 d) were evaluated: a control group (C2; n 6) was fed on a balanced diet (AIN-93G) and a fructose group (F2; n 6) was fed on a purified 60 % fructose diet. Finally, two young rat groups (aged 28 d) were analysed: a control group (C3; n 6) was fed on the AIN-93G diet and a fructose group (F3; n 6) was fed on a 60 % fructose diet. After 4-8 weeks, the animals were evaluated. Glucose tolerance, peripheral insulin sensitivity, blood lipid profile and body fat were analysed. In the fructose groups F2 and F3 glucose tolerance and insulin sensitivity were lower, while triacylglycerolaemia was higher than the respective controls C2 and C3 (P,0·05). Blood total cholesterol, HDL and LDL as well as body fat showed change only in the second protocol. In conclusion, high fructose intake is more effective at producing the signs of the metabolic syndrome in adult than in young Wistar rats. Additionally, diet seems to be a more effective way of fructose administration than drinking water.
Scripta scientifica medica, 2010
The global epidemic of metabolic syndrome (MS) correlates with changes in the environment, feeding, behavior and lifestyle, leading to obesity, glucose intolerans, dyslipidemià ànd elevated cardiovascular risk. AIM: The aim of our study was to develop an experimental model of the MS in rat that imitate the investigated metabolic disorders using high-fructose diet. METHODS: We used two groups: control group (C)-rats, maintained on plain water (n=6); fructose group (FRU)-rats received 12.5% high-fructose corn syrup in drinking water for 12 weeks (n=6). The main markers of metabolic abnormalities (glucose, total cholesterol, triglycerides, uric acid, body and organs weight), the markers of oxidative stress (malondialdehyde (MDA), total thiols) and C-reactive protein (CRP)-inflammatory marker were measured. RESULTS: Our data showed hypercholesterolemia, hyperglycemia, hyperuricemia and significant elevated levels of CRP, MDA, body and organs weight, and inhibited antioxidant defense in fructose-drinking rats. CONCLUSION: The experimental model will support our studies associated with pathophysiology and pharmacology of MS.
A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats
Brazilian Journal of Medical and Biological Research, 2001
Rats fed a high-fructose diet represent an animal model for insulin resistance and hypertension. We recently showed that a high-fructose diet containing vegetable oil but a normal sodium/potassium ratio induced mild insulin resistance with decreased insulin receptor substrate-1 tyrosine phosphorylation in the liver and muscle of normal rats. In the present study, we examined the mean blood pressure, serum lipid levels and insulin sensitivity by estimating in vivo insulin activity using the 15-min intravenous insulin tolerance test (ITT, 0.5 ml of 6 µg insulin, iv) followed by calculation of the rate constant for plasma glucose disappearance (K itt) in male Wistar-Hannover rats (110-130 g) randomly divided into four diet groups: control, 1:3 sodium/potassium ratio (R Na:K) diet (C 1:3 R Na:K); control, 1:1 sodium/potassium ratio diet (CNa 1:1 R Na:K); high-fructose, 1:3 sodium/potassium ratio diet (F 1:3 R Na:K), and high-fructose, 1:1 sodium/potassium ratio diet (FNa 1:1 R Na:K) for 28 days. The change in R Na:K for the control and high-fructose diets had no effect on insulin sensitivity measured by ITT. In contrast, the 1:1 R Na:K increased blood pressure in rats receiving the control and high-fructose diets from 117 ± 3 and 118 ± 3 mmHg to 141 ± 4 and 132 ± 4 mmHg (P<0.05), respectively. Triacylglycerol levels were higher in both groups treated with a high-fructose diet when compared to controls (C 1
SERUM LIPIDS AND LIPOPROTEINS OF WISTAR RATS WITH FRUCTOSE-INDUCED METABOLIC SYNDROME
Bayero Journal of Medical Laboratory Sciences, 2019
Background: Metabolic syndrome (MetS) is a combination of cardio-metabolic risk factors including obesity, hyperglycaemia, hypertriglyceridaemia, oxidative stress, dyslipidaemia, and hypertension. Aim: This study was aimed at evaluating the serum lipids and lipoprotein levels in Wistar rats with fructose-induced metabolic syndrome. Method: Twenty rats were randomly divided into two groups of 10 each: controlgroup on drinking water and standard rodent chow ad-libitum for 32 weeks andtest group treated with 10% fructose in drinking water (w/v) and standard rodent chow ad-libitum for 32 weeks. Baseline body weight, body mass index (BMI) and fasting plasma glucose (FPG) were measured. At the end of the experiment, the rats were fasted for 12 hours and blood samples collected under chloroform anaesthesia for the estimation of fasting serum lipid lipids, lipoproteins and plasma glucose. Data generated was analysed using statistical package for social sciences (SPSS) version 23. Results were expressed as mean ± standard error of mean for the rats in each group. Value of the variables were analysed using independent sample t-test while the differences were considered significant when P is equal to or less than 0.05 (p ≤ 0.05). Results: The results indicate significantly increased BMI and plasma glucose in MetS rats group compared to controls. The result also showed that with the exception of serum high density lipoprotein (HDL) which showed a significant decrease (p = 0.040), the levels of serum cholesterol (TC), lipoproteins (VLDL and LDL) and triglyceride (TG) significantly (p < 0. 001, p = 0.004 respectively) increase in MetS compared with controls, while serum atherogenic index (AIX) levels were similar in MetS rats and controls. Conclusion: The current study demonstrate that excessive fructose consumption alters serum lipids and lipoprotein fractions and plays an important role in the pathogenesis of components of metabolic syndrome, including dyslipidaemia, hyperglycaemia and obesity. Measurement of serum lipids and lipoprotein profile and other biochemical components of metabolic syndrome may provide cost-effective means for the recognition of a pathophysiological process and early identification of metabolic syndrome.
Fructose-Induced Insulin Resistance: Prospective Biochemical Mechanisms
Jordan Journal of Agricultural Sciences
Increased intake of dietary fructose is markedly associated with multiple negative health outcomes and burdens. Insulin resistance (IR) and type 2 diabetes mellitus (T2DM) are the most common complications that present with conjugated cellular-biochemical abnormalities. This article explains the involvement of increased dietary fructose intake in the occurrence of IR and T2DM and addresses basic metabolic mechanisms. PubMed, Medline, Science Direct, ADI, and WHO databases were searched through June 2021. Current research predicts that over 350 million people may have diabetes by 2030. IR acts as an influencer promoter of T2DM development. IR can occur as a result of high fructose intake. Fructose metabolism results in de novo lipogenesis, while its decreasing effect of peroxisome proliferator-activated receptor (PPAR) activity elevates the levels of inflammatory cytokines, resulting in down-regulation of insulin receptor substrate-1 phosphorylation. Fructose stimulates oxidative str...
Journal of Proteome Research, 2016
We aimed to determine the time-course of metabolic changes related to the early onset of insulin resistance (IR), trying to evidence breaking points preceding the appearance of the clinical IR phenotype. The model chosen was the fructose (FRU)-fed rat compared to controls fed with starch. We focused on the hepatic metabolism after 0, 5, 12, 30 or 45 days of FRU intake. The hepatic molecular metabolic changes followed indeed a multi-step trajectory rather than a continuous progression. After 5d of FRU, we observed deep modifications in the hepatic metabolism, driven by the induction of lipogenic genes and important glycogen depletion. Thereafter, a steady-state period between d12 and 30 was observed, characterized by a switch from carbohydrate to lipid utilization at the hepatic level and increased insulin levels aiming at alleviating lipid accumulation and hyperglycemia respectively. The FRU-fed animals were only clinically IR at d45 (altered HOMA-IR and muscle glucose transport). Further, the urine metabolome revealed even earlier metabolic trajectory changes that precede the hepatic alterations. We identified several candidate metabolites linked to the tryptophan-nicotinamide metabolism and the installation of fasting hyperglycemia that suggest a role of this metabolic pathway on the development of the IR phenotype in the FRU-fed rats.