The effects of glucose and fructose on body weight and some biochemical parameters in rats (original) (raw)
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Effects of fructose consumption on food intake and biochemical and body parameters in Wistar rats
Revista portuguesa de cardiologia : orgao oficial da Sociedade Portuguesa de Cardiologia = Portuguese journal of cardiology : an official journal of the Portuguese Society of Cardiology, 2017
Increased fructose consumption is associated with various metabolic changes that favor the onset of obesity and related comorbidities. The objective of this study was to assess the effects of chronic fructose consumption on body weight and adipose tissue, as well as on serum glucose and triglyceride levels. Thirty-day-old Wistar rats were divided into two groups: fructose (F) and control (C), which had free access to commercial chow and either water or a 20% fructose solution. Body mass was measured weekly and food consumption at 30, 60 and 90 days. At 90 days, the animals were killed by decapitation and fat deposits (mesenteric, epididymal and retroperitoneal) were removed and blood collected for measurement of glucose and triglyceride levels. There was no significant difference in body weight gain, but the percentage of body fat was higher in group F. This group also consumed less feed at 60 and 90 days and had higher consumption of fructose solution than water in group C at 30 an...
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.
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.
International journal of pharmaceutical sciences review and research, 2022
Consumption of high fructose is potently related to the development of hypertension and metabolic syndrome. This theory is supported by observational and experimental studies in animals and humans. Rising consumption of fructose has been matched with growing rates of hypertension and hyperglycemia. A high fructose diet has been found to activate vasoconstrictors and inactivate vasodilators. Salt reabsorption a reason for the increase in blood pressure is also shown by excess consumption of fructose. The fructose-taking diet in the rat causes modifications in the triglyceride concentrations in serum, liver TBARS, liver catalase, and SOD activity. In conclusion, the fructose diet caused significant liver damage and a reduction in insulin sensitivity.
Metabolic Effects of Fructose and the Worldwide Increase in Obesity
Physiological Reviews, 2010
While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been pr...
Fructose affects fatty acids profile in liver cells in vitro and in vivo models in rats
It was reported that dietary fructose imposes a number of effects on lipid metabolism including hypertriglyceridemia. The daily intake of fructose in humans is mainly due to sucrose. It was reported that the consumption is still increasing, making a background for health implications. The mechanism of metabolic disorders is poorly understood, but a lot of studies indicate that the liver lipid homeostasis deregulation is essential for a fructose effect on metabolism. The aim of the study is to estimate if fructose affects the profile of fatty acids in in vitro and in vivo models. In this study in vitro and in vivo experiments were conducted to assess the effect of dietary fructose on the fatty acid profile in the cell culture or in the liver of rats. The results showed that in the fructose experimental groups, both in the cell and liver homogenates, the content of the saturated fatty acids were significantly higher than in control groups. According to the obtained data fructose in the medium and in the diet affects saturation of fatty acids in the cell cultures and in the livers of rats. The findings obtained in the experiments support the thesis that fructose influences the homeostasis of lipid metabolism in the liver and may give an opportunity to discuss the limitation of the content of this kind of sugar in food.
Archives of Biological Sciences, 2019
An increase in fructose consumption coincides with a rising incidence of metabolic disorders. Dietary fructose has been shown to affect hepatic lipid metabolism in a way that may lead to lipid deposition in the liver. In this study, we tested the hypothesis that the effects of fructose overconsumption on hepatic lipid metabolism differ between sexes. To that end we examined the effects of a high-fructose diet on the expression of key enzymes and transcription factors involved in the regulation of fatty acid oxidation and de novo lipogenesis in the liver of 12-week-old male and female Wistar rats. Immediately after weaning, the rats were subjected to a standard diet and 10% fructose solution or drinking water for 9 weeks. The fructose-enriched diet induced hypertriglyceridemia and increased hepatic de novo lipogenesis in both sexes, without lipid deposition in the liver. At the same time, visceral adiposity was observed only in female rats, while in males the treatment stimulated hep...
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.