The metabolic syndrome of fructose-fed rats: Effects of long-chain polyunsaturated ω3 and ω6 fatty acids. IV. D-glucose metabolism by isolated pancreatic islets (original) (raw)
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Archives of Biochemistry and Biophysics, 2002
The metabolism of D D -glucose and/or D D -fructose was investigated in pancreatic islets from control rats and hereditarily diabetic GK rats. In the case of both D D -glucose and D D -fructose metabolism, a preferential alteration of oxidative events was observed in islets from GK rats. The generation of 3 HOH from D D -[5-3 H]glucose (or D D -[5-3 H]fructose) exceeded that from D D -[3-3 H]glucose (or D D -[3-3 H]fructose) in both control and GK rats. This difference, which is possibly attributable to a partial escape from glycolysis of tritiated dihydroxyacetone phosphate, was accentuated whenever the rate of glycolysis was decreased, e.g., in the absence of extracellular Ca 2þ or presence of exogenous D D -glyceraldehyde. D D -Mannoheptulose, which inhibited D D -glucose metabolism, exerted only limited effects upon D D -fructose metabolism. In the presence of both hexoses, the paired ratio between D D -[U-14 C]fructose oxidation and D D -[3-3 H]fructose or D D -[5-3 H]fructose utilization was considerably increased, this being probably attributable, in part at least, to a preferential stimulation by the aldohexose of mitochondrial oxidative events. Moreover, this coincided with the fact that D D -mannoheptulose now severely inhibited the catabolism of D D -[5-3 H]fructose and D D -[U-14 C]
The Journal of Nutritional Biochemistry, 1995
The aim of the present study was to investigate under controlled conditions the in vitro metabolic effects of fructose and insulin on the triglyceride formation by the isolated perfused livers obtained from hypertriglyceridemic rats that had been fed a sucrose-rich diet for a long-term (15 week) period as compared with those fed sucrose for a short-term (3 week) period. Our findings indicate a significantly higher increase in triglyceride formation by perfused livers of rats fed the sucrose-rich diet for a long-term period in the presence of oleate as a triglyceride-forming substrate (15 weeks, 6-fold increase; 3 weeks, Z-fold increase). Though the contribution of net triglyceride secretion to this increase in triglyceride formation was about twice as high at both durations of feeding on a sucrose-rich diet, a strikingly elevated liver triglyceride accumulation was recorded for a long-term period (15 week, IO-fold increase; 3 week, 4-fold increase). The addition offructose in the petfusate further increased the output of triglycerides from livers of animals fed the sucrose diet at both durations of feeding. Despite this finding, long-term sucrose led to even higher hepatic triglyceride storage under the present experimental conditions (+mollliver at 15 week; 318.2 + 17.2 vs. 63.0 + 10.0 at 3 week; P < 0.001). Insulin in the presence of fructose promoted synthesis of liver triglycerides at both durations of feeding on the sucroserich diet. However, dtzerent insulin responses have been observed, showing an increase (3-fold) in triglyceride storage only in rats fed the sucrose diet for 3 weeks and an inhibition (320/o) on the net triglyceride output only in animals fed the sucrose diet for 15 weeks. Our findings indicate important differences in the in vitro effects of fructose and insulin on hepatic triglyceride formation characterized by an imbalance between secretion and storage depending on the duration of feeding on the sucrose-rich diet. Thus care should be taken when generalizing conclusions on the eflects of nutrients or hormones in this nutritionally induced hyperlipemic experimental animal model, since variable metabolic milieu may emerge at different durations offeeding on the diet. (J. NW. B&hem. 6:422-430, 1995.) . erides in both humans and experimental animals. Id3 Until the present time, most of the available animal studies on the mechanisms underlying carbohydrate-induced hypertriglyceridemia were conducted in short-or medium-term (a few weeks) trials.3-7 Studies on the long-term metabolic consequences of high carbohydrate feeding are limited,&' t and, particularly, those concerning very low density lipoproteintriglycerides (VLDL-TG) secretion and removal are contradictory.8%9 Thus Schonfeld et a1.9 showed a rise of in vitro VLDL-TG output by livers obtained from rats fed fructose Nutritional Biochemistry 6:422-430, 1995 0 Elsevier Science Inc. 1995 Effect of sucrose intake on liver triglyceride metabolism: Bernal et al.
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.
High-fructose diet stimulates hepatic de novo lipogenesis (DNL) and causes hypertriglyceridemia and insulin resistance in rodents. Fructose-induced insulin resistance may be secondary to alterations of lipid metabolism. In contrast, fish oil supplementation decreases triglycerides and may improve insulin resistance. Therefore, we studied the effect of high-fructose diet and fish oil on DNL and VLDL triglycerides and their impact on insulin resistance. Seven normal men were studied on four occasions: after fish oil (7.2 g/day) for 28 days; a 6-day high-fructose diet (corresponding to an extra 25% of total calories); fish oil plus high-fructose diet; and control conditions. Following each condition, fasting fractional DNL and endogenous glucose production (EGP) were evaluated using [1-13C]sodium acetate and 6,6-2H2 glucose and a two-step hyperinsulinemic-euglycemic clamp was performed to assess insulin sensitivity. High-fructose diet significantly increased fasting glycemia (7 +/- 2%), triglycerides (79 +/- 22%), fractional DNL (sixfold), and EGP (14 +/- 3%, all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). It also impaired insulin-induced suppression of adipose tissue lipolysis and EGP (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) but had no effect on whole- body insulin-mediated glucose disposal. Fish oil significantly decreased triglycerides (37%, P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) after high-fructose diet compared with high-fructose diet without fish oil and tended to reduce DNL but had no other significant effect. In conclusion, high-fructose diet induced dyslipidemia and hepatic and adipose tissue insulin resistance. Fish oil reversed dyslipidemia but not insulin resistance.
Long-term high fructose and saturated fat diet affects plasma fatty acid profile in rats
Journal of Zhejiang University SCIENCE B, 2012
As the consumption of fructose and saturated fatty acids (FAs) has greatly increased in western diets and is linked with an increased risk of metabolic syndrome, the aim of this study was to investigate the effects of a moderate (10 weeks) and a prolonged (30 weeks) high fructose and saturated fatty acid (HFS) diet on plasma FA composition in rats. The effects of a few weeks of HFS diet had already been described, but in this paper we tried to establish whether these effects persist or if they are modified after 10 or 30 weeks. We hypothesized that the plasma FA profile would be altered between 10 and 30 weeks of the HFS diet. Rats fed with either the HFS or a standard diet were tested after 10 weeks and again after 30 weeks. After 10 weeks of feeding, HFS-fed rats developed the metabolic syndrome, as manifested by an increase in fasting insulinemia, total cholesterol and triglyceride levels, as well as by impaired glucose tolerance. Furthermore, the plasma FA profile of the HFS group showed higher proportions of monounsaturated FAs like palmitoleic acid [16:1(n-7)] and oleic acid [18:1(n-9)], whereas the proportions of some polyunsaturated n-6 FAs, such as linoleic acid [18:2(n-6)] and arachidonic acid [20:4(n-6)], were lower than those in the control group. After 30 weeks of the HFS diet, we observed changes mainly in the levels of 16:1(n-7) (decreased) and 20:4(n-6) (increased). Together, our results suggest that an HFS diet could lead to an adaptive response of the plasma FA profile over time, in association with the development of the metabolic syndrome.
Diabetes, 2005
High-fructose diet stimulates hepatic de novo lipogenesis (DNL) and causes hypertriglyceridemia and insulin resistance in rodents. Fructose-induced insulin resistance may be secondary to alterations of lipid metabolism. In contrast, fish oil supplementation decreases triglycerides and may improve insulin resistance. Therefore, we studied the effect of high-fructose diet and fish oil on DNL and VLDL triglycerides and their impact on insulin resistance. Seven normal men were studied on four occasions: after fish oil (7.2 g/day) for 28 days; a 6-day high-fructose diet (corresponding to an extra 25% of total calories); fish oil plus high-fructose diet; and control conditions. Following each condition, fasting fractional DNL and endogenous glucose production (EGP) were evaluated using [1-13C]sodium acetate and 6,6-2H2 glucose and a two-step hyperinsulinemic-euglycemic clamp was performed to assess insulin sensitivity. High-fructose diet significantly increased fasting glycemia (7 +/- 2%), triglycerides (79 +/- 22%), fractional DNL (sixfold), and EGP (14 +/- 3%, all P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05). It also impaired insulin-induced suppression of adipose tissue lipolysis and EGP (P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) but had no effect on whole- body insulin-mediated glucose disposal. Fish oil significantly decreased triglycerides (37%, P &amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; 0.05) after high-fructose diet compared with high-fructose diet without fish oil and tended to reduce DNL but had no other significant effect. In conclusion, high-fructose diet induced dyslipidemia and hepatic and adipose tissue insulin resistance. Fish oil reversed dyslipidemia but not insulin resistance.
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.
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, ...
Adaption of Sprague Dawley rats to long-term feeding of high fat of high fructose diets
European Journal of Nutrition, 2000
Background Present animal models used to emulate type 2 diabetes may not accurately reflect the metabolic changes that occur in humans. Aim of the study The purpose of this research was to evaluate diets reported to induce insulin resistance and impaired glucose metabolism in rats as a potentially useful model for studying type 2 diabetes. Methods Three groups of male Sprague Dawley rats (n=7) were fed either a control diet, based on AIN recommendations (53 % cornstarch, 10 % sucrose and 7 % soybean oil), a high fat diet (25 % soybean oil, 35 % cornstarch) or a high fructose diet (53 % fructose, 10 % sucrose) for a 3 month period. Glucose tolerance tests were carried out in week 3 and week 9 of the experiment. At the termination of the experiment, serum insulin, glucose, cholesterol and triacylglycerols were measured. Glucose incorporation into glycogen and glycogen synthase activity were measured in soleus muscles. Results Similar weight gain was observed for all three groups of rats. Glucose tolerance curves and fasting glucose levels were not significantly different at any time point in the experiment. Insulin levels were unchanged for the controls (171±21 pM), high fructose (164±16 pM) and high fat (181±30 pM) diets. Fasting serum triacylglycerols and cholesterol levels were not significantly elevated by dietary treatment. In soleus muscles, rats on all three diets had a significant increase in glycogen synthesis in response to insulin, but synthesis was similar in all three groups. Glycogen synthase activity was also not significantly affected by long-term dietary intervention. Conclusions In this study, healthy Sprague Dawley rats fed high fat or high fructose diets for 3 months adapted to the nutritional intervention without developing classical signs of insulin resistance and impaired glucose tolerance.