Neither dietary fructose, dextrose nor starch modifies in vitro glycerol release by adipocytes from streptozotocin-diabetic rats (original) (raw)
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To study the cellular mechanisms under lying fructose-induced insulin resistance in rats, the ef fects of fructose feeding on insulin-stimulated glucose transport, oxidation and incorporation into lipids in epididymal adipocytes were evaluated in 27 normal and 27 noninsulin-dependent diabetic male Sprague-Dawley rats. Diabetes was induced by streptozotocin injection 2 d after birth. At 5 wk of age, both normal and diabetic rats were fed a diet containing 62% carbohydrate as fructose, dextrose or cornstarch. Fructose feeding for 6 wk induced glucose intolerance in normal rats (P < 0.05) and aggravated that of diabetic rats (P < 0.05). Plasma triacylglycerol concentration was higher in fructose-fed than in starch-fed or dextrose-fed rats (P < 0.05). Adipocytes of fructose-fed rats had significantly lower maximum insulin-stimulated glucose incorporation into total lipids than those of rats fed starch, and tended (P = 0.22) to have lower production of CÃ'2 from glucose than adipocytes of the other dietary groups. Glucose transport in adipocytes of dextrose-, starch-and fructose-fed rats did not differ. We conclude that in both normal and diabetic rats, a chronic fructose-rich diet induced hypertriacylglycerolemia, glucose intolerance and insulin resistance of adipocytes. J. Nutr. 125: 164-171, 1995.
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, ...
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.
International Journal of Molecular Medicine, 2011
The major aim of the present study was to search for changes of D-glucose metabolism in isolated pancreatic islets possibly involved in the alteration of their secretory response to the hexose, as observed when comparing rats exposed for 8 weeks to diets containing either starch and sunflower oil or fructose and sunflower oil, as well as rats exposed to diets containing fructose, sunflower oil and either salmon oil or safflower oil. The substitution of starch by fructose in the diet affected unfavourably D-glucose phosphorylation by the isolated islets. In the fructose-fed rats, there was a close parallelism between D-[5-3 H]glucose utilization and the dietary ω3/ω6 fatty acid ratio. There was little to distinguish, however, between the four groups of rats in terms of D-[U-14 C]glucose oxidation. The paired ratio between D-[U-14 C]glucose oxidation and D-[5-3 H]glucose utilization, which always increased as the concentration of the hexose was raised from 2.8 to 8.3 and 16.7 mM, was tightly related, in the fructose-fed rats, to the HOMA index for insulin resistance.
The effects of glucose and fructose on body weight and some biochemical parameters in rats
Progress in Nutrition, 2018
Objective: Dietary fructose from added sugar as high fructose corn syrup may causes major risks in obesity, hyperlipidemia, cardiovascular diseases, hyperuricemia and fatty liver. The aim of this study was to investigate and compare the effects of high fructose and high glucose intake on body weight and some biochemical parameters in rats. Subject and methods: The study was conducted on adult, 32 Wistar albino male rats (300-350 g weeks) which fed with standard laboratory chow. In each group, 8 rats was selected randomly and which was be composed four groups. The rats in each group, in addition to standard meal, different amount of glucose and fructose containing solutions (10% and 30% glucose-fed group, 10% and 30% fructose-fed group) was given by oral gavage for 6 weeks. At baseline and after 6 weeks total cholesterol, VLDL-cholesterol, triglycerides, uric acid, AST and ALT as biochemical parameters and liver histopathological examination of rats were determined. Body weight of t...
Mechanisms for the acute effect of fructose on postprandial lipemia
The American Journal of Clinical Nutrition, 2007
Background: A high fructose intake can lead to postprandial hypertriacylglycerolemia. The underlying mechanism is unclear. Objective: The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting. Design: In a randomized, crossover study, 14 subjects were given a fructose or glucose test meal after an overnight fast. [ 2 H 2 ]Palmitate and [U 13 C]D-fructose or [U 13 C]D-glucose were added to trace the handling of dietary fats and the fate of dietary sugars in the body. Blood samples were taken before and after the meal. Respiratory exchange ratio was measured by using indirect calorimetry, and breath samples were collected. Results: Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher (P ҃ 0.001 for both), whereas the concentrations of insulin and [ 2 H 2 ]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose (P ҃ 0.002 and 0.03, respectively). The respiratory exchange ratio was higher after fructose (P ҃ 0.04); significantly (P ҃ 0.003) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose (30.5%) than after glucose (24.5%). At 240 min, newly synthesized fatty acids from fructose made up Ȃ0.4% of circulating VLDL-triacylglycerol, whereas newly synthesized triacylglycerolglycerol made up 38%. Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol (P ҃ 0.002 and 0.007 for glucose and fructose, respectively). Conclusions: The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase, which led to impaired triacylglycerol clearance. The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small, but its effect on altering the partitioning of fatty acids toward esterification may be considerable.
Cultured adipocytes (3T3-L1) produce large amounts of 3C fragments; largely lactate, depending on medium glucose levels. Increased glycolysis has been observed also in vivo in different sites of rat white adipose tissue. We investigated whether fructose can substitute glucose as source of lactate, and, especially whether the glycerol released to the medium was of lipolytic or glycolytic origin. Fructose conversion to lactate and glycerol was lower than that of glucose. The fast exhaustion of medium glucose was unrelated to significant changes in lipid storage. Fructose inhibited to a higher degree than glucose the expression of lipogenic enzymes. When both hexoses were present, the effects of fructose on gene expression prevailed over those of glucose. Adipocytes expressed fructokinase, but not aldolase b. Substantive release of glycerol accompanied lactate when fructose was the sub-strate. The mass of cell triacylglycerol (and its lack of change) could not justify the comparatively higher amount of glycerol released. Consequently, most of this glycerol should be derived from the glycolytic pathway, since its lipolytic origin could not be (quantitatively) sustained. Proportionally (with respect to lactate plus glycerol), more glycerol was produced from fructose than from glucose, which suggests that part of fructose was catabolized by the alternate (hepatic) fructose pathway. Earlier described adipose glycerophophatase activity may help explain the glycolytic origin of most of the glycerol. However, no gene is known for this enzyme in mammals, which suggests that this function may be carried out by one of the known phosphatases in the tissue. Break up of glycerol-3P to yield glycerol, may be a limiting factor for the synthesis of triacylglycerols through control of glycerol-3P availability. A phosphatase pathway such as that described may have a potential regulatory function, and explain the production of glycerol by adipocytes in the absence of lipolytic stimulation.
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.