A high-fructose diet induces insulin resistance but not blood pressure changes in normotensive rats (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, ...
Lipid profile and insulin sensitivity in rats fed with high-fat or high-fructose diets
British Journal of Nutrition, 2011
The occurrence and severity of obesity-and insulin resistance-related disorders vary according to the diet. The aim of the present longitudinal study was to examine the effects of a high-fat or a high-fructose diet on body weight (BW), body fat mass, insulin sensitivity (IS) and lipid profiles in a rat model of dietary-induced obesity and low IS. A total of eighteen, 12-week-old male Wistar rats were divided into three groups, and were fed with a control, a high-fat (65 % lipid energy) or a high-fructose diet (65 % fructose energy) for 10 weeks. BW, body fat mass ( 2 H 2 O dilution method), IS (euglycaemic -hyperinsulinaemic clamp technique), plasma glucose, insulin, NEFA, TAG and total cholesterol were assessed before and at the end of 10-week period. Cholesterol was measured in plasma lipoproteins separated from pooled samples of each group and each time period by using fast-protein liquid chromatography. All rats had similar BW at the end of the 10-week period. Body fat mass was higher in the high-fat group compared to the control group. There was no change in basal glycaemia and insulinaemia. The IS was lower in the high-fat group and was unchanged in the high-fructose group, compared to the control group. Plasma TAG concentration and cholesterol distribution in lipoproteins did not change over time in any group. Plasma NEFA concentration decreased, whereas plasma TAG concentration increased over time, regardless of the diet in both cases. The 10-week high-fat diet led to obesity and low IS, whereas rats fed with the high-fructose diet exhibited no change in IS and lipidaemia. The high-fat diet had more deleterious response than high-fructose diet to induce obesity and low IS in rats.
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.
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.
The American journal of clinical nutrition, 2006
High fructose consumption is suspected to be causally linked to the epidemics of obesity and metabolic disorders. In rodents, fructose leads to insulin resistance and ectopic lipid deposition. In humans, the effects of fructose on insulin sensitivity remain debated, whereas its effect on ectopic lipids has never been investigated. We assessed the effect of moderate fructose supplementation on insulin sensitivity (IS) and ectopic lipids in healthy male volunteers (n = 7). IS, intrahepatocellular lipids (IHCL), and intramyocellular lipids (IMCL) were measured before and after 1 and 4 wk of a high-fructose diet containing 1.5 g fructose . kg body wt(-1) . d(-1). Adipose tissue IS was evaluated from nonesterified fatty acid suppression, hepatic IS from suppression of hepatic glucose output (6,6-2H2-glucose), and muscle IS from the whole-body glucose disposal rate during a 2-step hyperinsulinemic euglycemic clamp. IHCL and IMCL were measured by 1H magnetic resonance spectroscopy. Fructos...
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.
Fructose Metabolism and Relation to Atherosclerosis, Type 2 Diabetes, and Obesity
Journal of nutrition and metabolism
A high intake of sugars has been linked to diet-induced health problems. The fructose content in sugars consumed may also affect health, although the extent to which fructose has a particularly significant negative impact on health remains controversial. The aim of this narrative review is to describe the body's fructose management and to discuss the role of fructose as a risk factor for atherosclerosis, type 2 diabetes, and obesity. Despite some positive effects of fructose, such as high relative sweetness, high thermogenic effect, and low glycaemic index, a high intake of fructose, particularly when combined with glucose, can, to a larger extent than a similar glucose intake, lead to metabolic changes in the liver. Increased de novo lipogenesis (DNL), and thus altered blood lipid profile, seems to be the most prominent change. More studies with realistic consumption levels of fructose are needed, but current literature does not indicate that a normal consumption of fructose (approximately 50-60 g/day) increases the risk of atherosclerosis, type 2 diabetes, or obesity more than consumption of other sugars. However, a high intake of fructose, particularly if combined with a high energy intake in the form of glucose/starch, may have negative health effects via DNL.
Gastroenterology, 2013
BACKGROUND & AIMS: Diets high in fructose have been proposed to contribute to nonalcoholic fatty liver disease. We compared the effects of high-fructose and matched glucose intake on hepatic triacylglycerol (TAG) concentration and other liver parameters. DESIGN: In a double-blind study, we randomly assigned 32 healthy but centrally overweight men to groups that received either a high-fructose or high-glucose diet (25% energy). These diets were provided during an initial isocaloric period of 2 weeks, followed by a 6-week washout period, and then again during a hypercaloric 2-week period. The primary outcome measure was hepatic level of TAG, with additional assessments of TAG levels in serum and soleus muscle, hepatic levels of adenosine triphosphate, and systemic and hepatic insulin resistance. RESULTS: During the isocaloric period of the study, both groups had stable body weights and concentrations of TAG in liver, serum, and soleus muscle. The high-fructose diet produced an increase of 22 AE 52 mmol/L in the serum level of uric acid, whereas the high-glucose diet led to a reduction of 23 AE 25 mmol/L (P < .01). The high-fructose diet also produced an increase of 0.8 AE 0.9 in the homeostasis model assessment of insulin resistance, whereas the high-glucose diet produced an increase of only 0.1 AE 0.7 (P ¼ .03). During the hypercaloric period, participants in the high-fructose and high-glucose groups had similar increases in weight (1.0 AE 1.4 vs 0.6 AE 1.0 kg; P ¼ .29) and absolute concentration of TAG in liver (1.70% AE 2.6% vs 2.05% AE 2.9%; P ¼ .73) and serum (0.36 AE 0.75 vs 0.33 AE 0.38 mmol/L; P ¼ .91), and similar results in biochemical assays of liver function. Body weight changes were associated with changes in liver biochemistry and concentration of TAGs. CONCLUSIONS: In the isocaloric period, overweight men who were on a high-fructose or a high-glucose diet did not develop any significant changes in hepatic concentration of TAGs or serum levels of liver enzymes. However, in the hypercaloric period, both high-fructose and high-glucose diets produced significant increases in these parameters without any significant difference between the 2 groups. This indicates an energymediated, rather than a specific macronutrientmediated, effect. Clinical trials.gov no: NCT01050140.