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Affect on weight gain and sugar water on Mice - Research Paper Example

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For the past few decades, obesity is the major epidemic problem in many countries around the world. World Health Organization says that around 1 billion are above the normal weight and the body mass index is greater than 25…
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Affect on weight gain and sugar water on Mice
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? Affect on weight gain and sugar water on Mice Introduction: For the past few decades, obesity is the major epidemic problem in many countries around the world. World Health Organization says that around 1 billion are above the normal weight and the body mass index is greater than 25. (Malik, Schulze and Hu). In addition, nearly 25% of the overweight persons are obese, with most of the overweight persons are in the age group 20 – 70 years. (Malik, Schulze and Hu). Overweight and obesity are interrelated terms for many health complications. Children and adolescents also fall under this category. Many health complications such as diabetes, cardiovascular disease, hypertension, breast, colon and prostate cancers and depression are associated with the obesity and overweight. (Malik, Schulze and Hu). Obesity is caused due to the imbalance in the energy homeostasis. Many factors such as metabolic, environmental, cultural, socioeconomic, genetic and behavioral factors are associated with the obesity and overweight. The reason for the increase in the body weight was identified as increased carbohydrate intake mainly in the form of sugars. Carbohydrate intake increases the blood glucose and insulin levels. If simple carbohydrates are taken in the food, the production of glucose is very high and it increases the blood glucose level. Undigestable carbohydrates do not increase the blood glucose level as that of simple sugar and simple carbohydrates. This sort of hyperglycemic response increases the carbohydrate oxidation and contributes to the body fat gain. (Malik, Schulze and Hu). The sudden changes in the blood glucose contribute to the variation in the postprandial glucose concentration. This finally affects the metabolism of the body and induces weight gain. Our body can store 300-500g of carbohydrates as glycogen in the human body and the rest are oxidized and converted into fat. The studies have confirmed that a 480g of oral carbohydrate load did not induce the fat oxidation in the young adults. (Saris). If the percentage of carbohydrate intake is very high then the increase in the body weight will be drastic. The increase in the body weight also leads to the risk of coronary heart disease and Type 2Diabetes mellitus. Obesity is generally caused by the difference in the energy homeostasis of food intake and daily physical activity. Obesity is the nutrition related problem in the developing and developed countries. To overcome obesity, many health guidelines are focused such as increase in the physical activity and reducing the intake of foods containing sugar and fat. Sugar is a disaccharide molecule. Sucrose, maltose and lactose are compound sugars with the general formula C12H22O11 . (Saris). Sucrose is the common sugar used in our day to day life. Sucrose contains glucose and fructose. Sucrose is the most important dietary factor for weight gain. Readily digestible food have high glycemic index( GI) with higher post prandial blood glucose and insulin concentrations than the less digestible carbohydrates. Sugar containing foods have high glycemic index and increase the carbohydrate oxidation and contribute to body weight. (Saris). Similarly high fructose and galactose content increases the body weight. The galactose and fructose are used as sweeteners in the food and they increase the blood glucose concentration on ingestion. The sweet taste of the sugar is the main reason for the preference and intake of carbohydrate rich food. Diet induced obesity is caused by the conversion of carbohydrates into fat deposits in the white adipose tissue and the liver. (Lowndes et al.). The energy metabolism and carbohydrate and lipid metabolism are regulated by a complex network of signaling processes. High sucrose diet can induce the expression of the white adipose tissue and mRNA of liver Lipoprotein lipase enzyme. High sucrose diet is found to increase the risks of cancer. Pancreatic cancer is the most pre dominant cancer in this case. The diet that contains high concentration of sucrose and dextrin acts as the promoter for cancer development. They are also found to cause malignant tumors in the colon. The glycemic load is a risk factor for pancreatic cancer. The risk of esophageal adenocarcinoma is also associated with the small intestinal cancer. Lipid peroxidation is the main factor to release the free radicals in the biological membranes. (Lowndes et al.). The unsaturation of the fatty acids determines the susceptibility to the peroxidation. The presence of lipid molecules in the diet will affect the fatty acid composition in the membrane. (Lowndes et al.). Glutathione is the tripeptide that is found to regulate the biological processes such as DNA synthesis, signal transduction, antioxidant defenses, enzyme activity and transcription. (Lowndes et al.). The decrease in the Glutathione increases the oxidative stress in the body. The decrease in the Glutathione (GSH) increases the accumulation of oxidized glutathione (GSSG). The accumulation of GSSG impairs the cellular functions. Oxidative stress due to high sucrose intake finally leads to lipid peroxidation. The fructose produced by the sucrose is the main factor for the harmful oxidative stress. Fructose has the stronger reducing capacity than the glucose and the glycation reaction is induced by the fructose. The oxidative stress of fructose alters the transcriptional factors and changes the redox state of the cell. Another important factor of high sucrose intake is the increased requirement for the vitamin E which is the most important free radical and lipid soluble molecule. Vitamin E is the major radical chain breaking component and an anti oxidant found in the cells and tissues that have decreasing blood level. The researches have thus concluded to use antioxidants with the dietary sucrose for preventing the oxidative stress and the oxidative ability. (Yang et al.). Research design and Method: A total of 11 mice were taken for the given study. Two mice were considered as control mice. The control mice are the normal mice. 2% sugar solution is the solution of 2 grams of sugar in water. Similarly 4% and 6% sugar solution were also prepared and used for the study. 3 mice each were used for the 2%, 4% and 6% sugar solution. The initial weights of the mice were analyzed and the weights of the mice were calculated at each week interval. At the end of 5 week, total weights gained by the mice were analyzed and the average weights are calculated. Result: Mice Initial weight (grams) Week 1 Week 2 Week 3 Week 4 Week 5 Total weight gain (grams) Average weight gain (grams) (grams) (grams) (grams) (grams) (grams) c1 25 26 29 34 34 34 9   c2 9 12 14 15 21 21 12 10.5 2m1 25 25 26 27 28 28 3   2m2 26 26 27 27 28 29 3   2m3 12 15 15 19 22 24 12 6 4m1 22 28 31 33 34 35 13   4m2 19 32 34 34 34 37 18   4m3 21 24 24 29 28 29 8 13 6m1 34 34 36 42 42 42 8   6m2 14 19 20 26 28 30 16   6m3 24 25 26 28 28 30 6 10 Table 1: Weight gain of test and control mice with sugar and no sugar solution. Figure 1: The Bar chart for weight gain in the test and control mice with sugar and no sugar solution. Sugar Water Average consumption C1 5 0 10 10 5 20 10 0 0 0 10 0 10 7 13 17 7.31 C2 5 10 10 30 5 15 5 0 10 10 20 5 5 10 0 20 10 2M1 10 0 0 5 5 5 10 0 4 6 20 4 10 5 5 5 5.88 2M2 10 0 0 0 0 25 5 2 2 8 20 0 0 9 1 9 5.69 2M3 3 5 0 0 0 10 5 10 3 7 15 0 10 5 15 5 5.81 4M1 5 2 0 13 0 20 10 15 8 12 10 11 10 11 9 20 9.75 4M2 5 0 0 0 10 20 10 10 5 5 5 0 0 13 0 20 6.44 4M3 5 0 0 0 7 28 10 5 7 13 20 0 5 8 12 8 8 6M1 5 10 0 25 5 20 10 10 13 7 30 5 0 11 0 20 10.7 6M2 30 5 0 5 10 10 0 0 3 7 15 0 0 4 1 9 6.19 6M3 15 10 0 30 12 8 10 5 6 4 10 0 0 6 4 16 8.5 Table 2: The sugar water consumption of the control and test mice (2%, 4% and 6% sugar solution fed mice respectively).. Figure 2: The average sugar water consumption chart of control and test mice (2%, 4% and 6% sugar solution fed mice respectively). .Mice Average water consumption C1 8.064516 C2 7.28125 2M1 8.151515 2M2 6.757576 2M3 6.515152 4M1 8.181818 4M2 9.090909 4M3 7.333333 6M1 7.545455 6M2 6.484848 6M3 6.30303 Table 3: the normal drinking water consumption of control and test mice (2%, 4% and 6% sugar solution fed mice respectively). Figure 3: The regular drinking water consumption of the control mice and test mice. (2%, 4% and 6% sugar solution fed mice respectively). Discussion: In the present study, the normal mice were obtained. 2 mice were treated as control and they were fed with only normal water. The other mice were fed with sugar solution at a concentration of 2%, 4% and 6% respectively for 5 weeks regularly. The initial weights of the mice were noted and the weight of the mice was checked at a week interval. After the end of the fifth week, the increase in the weight was calculated and the weight gained by the mice were calculated for control, 2% sugar solution, 4% sugar solution and 6% sugar solution respectively. It was observed that the mice weight increased with the increase in the concentration of the sugar solution. The control mice were very normal and the weight gain was similar to the 6% sugar solution fed mice. The 4% sugar solution fed mice was very active and was running throughout. The mice fed with 4% sugar solution obtained the maximum weight gain. The average weight gain was 13 grams. The 2% sugar solution fed mice had an average weight gain of 6 grams and this is very less when compared to the control mice. The regular water intake of control mice and test mice were analyzed. It was found that the normal drinking water was utilized by all the mice. On the average all the mice had an intake of 6 ml. The 4% sugar solution fed mice intake of normal drinking water was slightly high than the other mice and control. The average drinking water consumption of control mice was 8, 7.2 ml, 2% sugar solution fed mice was 8.1, 6. 75 and 6.2 respectively, 4% sugar solution fed mice was 8.1, 9.0 and 7.3 respectively, 6% sugar solution fed mice was 7.5, 6.4 and 6.3 respectively. The sugar solution was utilized by the test mice. It was observed that the quantity of the sugar solution intake varied between the test and the control and within the test mice also. The control mice had an average sugar water consumption of 7.3 ml and 10 ml respectively, 2% sugar solution fed mice had an intake of 5.9 ml, 5.8 ml and 5.7 ml respectively, 4% sugar solution fed mice intake was 9.75ml, 6.4 ml and 8 ml, 6% sugar solution fed mice intake was 10.7ml, 6.2 ml and 8.5 ml respectively. It was observed that the quantity of sugar solution intake was higher for the 6% sugar solution fed mice. These mice utilized almost the same amount of normal drinking water and sugar solution. 4% sugar solution fed mice utilized more amounts of normal drinking water and less amount of sugar solution. The control mice utilized the same amount of normal and sugar solution. 2% sugar solution fed mice fed more on normal drinking water and less on sugar solution. These data suggest that the sugar solution was well utilized by the less active mice than the more active mice. The sugar solution was given lesser importance by the 4% and 2% sugar solution fed mice. The control utilized more drinking water and less sugar solution indicating that the sweetness of the sugar was not welcomed by the normal mice. The same data continued till the end of the 5th week. Since the amount of sugar solution was very high and drinking water concentration was low in the 6% sugar solution fed mice, the rate of weight gain, increase in the body mass index, oxidative stress and the increase in the triglyceride concentration were very high in them. The mice gained more weight because of high calorie intake. The other mice had an average calorie intake and the weight gain was less compared to the 6% sugar solution fed mice. If the calorie intake is similar, then the high sucrose diet and standard diet will increase the body weight at the same rate. By feeding the high sucrose diet, the triglyceride concentration will increase along with stress tolerance. The use of high sucrose diet will increase the expression of the heat shock proteins HSP70 and HSP27 and will suppress the NOx production at the brain. This will not occur during the standard diet intake. If the calorie intake is correct, then there will be no increase in the body weight nor will obesity occur. The possible deleterious effect of high sucrose intake will be the stress and increase in the stress tolerance. (Kanazawa et al.). High sucrose diet will increase hyperphagia and affect the appetite and centers around the hypothalamus. Neuropeptide Y and Proopinne melanocortin are the two molecules that receive the nutritional status of the body and the energy storage. The insulin signaling and leptin signals are mediated by the receptors of proopinne melanocortin (POMC) and Neuropeptide Y (NPY) neurons. The NPY mRNA was down regulated and the hypothalamic mRNA is up regulated during the high sucrose intake. (Yang et al.). On the sugar intake for 5 weeks, the Body weight gain and Body mass index increase are due to the increase in the calorie intake. This increase in the calorie intake of carbohydrate has resulted in the increase of the adipose tissue deposition. The high sucrose intake will also result in the dysfunction of mitochondria at the adipose tissue. The mitochondrial dysfunction will cause metabolic impairment and increase weight gain. If the calorie intake is high for the obese patients, then fat mass, blood pressure and body weight increases. (Preedy). Sucrose intake will affect the dopamine system and increase the neurotransmitter dopamine, which alters the roles in behavior and mood. De novo lipogenesis plays a major role in the adiposity based on the response to carbohydrate feeding in the mice. Sucrose diet also increases the plasma triglycerides from the glucose and transports it to the adipose tissue. In the humans, sucrose is used in the artificial foods and beverages. They produce large amounts of glucose and fructose and are transported to the liver through the hepatic portal vein. Fructose by passes the hepatic glycolysis and enhances the fatty acid biosynthesis. Fatty acids esterification and increased serum triacylglycerols and VLDL secretion are the main effects of fructose in the blood. (Preedy). The study thus concludes that high sugar intake increases the weight gain, triacyl glyceride level in the blood and in turn oxidative stress and cellular dysfunction. These complications may lead to obesity, type 2 Diabetes mellitus and many types of cancer. The 6% sugar solution fed mice became obese in 5 weeks because of high calorie intake. References: Lowndes, Joshua., Diana Kawiecki, Sabrina Pardo, Von Nguyen, Kathleen J Melanson, Zhiping Yu and James M Rippe. The Effects of Four Hypocaloric Diets containing different levels of Sucrose or High Fructose Corn Syrup on Weight Loss and related Parameters. Nutritional journal 11.55 (2012). Kanazawa, Masao, Chang Young Xue, Haruaki Kageyama, Eiji Suzuki, Rokuro Ito, Yoshio Namba, Toshimasa Osaka, Shuichi Kimura and Shuji Inoue. Effects of a High –Sucrose Diet on Body Weight, Plasma Gycerides and Stress Tolerance. Nutrition Reviews 61. 5 (2003): S27 – S33. Malik, Vasanti S., Matthias B Schulze and Frank B. Hu. Intake of Sugar –Sweetened Beverages and Weight Gain: a Systematic Review. The American Journal of Clinical Nutrition 84.2 (2006): 274- 288. Preedy, Victor R. Dietary Sugars: Chemistry, Analysis, Function and Effects, Royal Society of chemistry, 2012. Saris, WHM. Sugars, Energy Metabolism and Body Weight Control, The American Journal of Clinical Nutrition. 78.4 (2003): 8505-8575. Yang, Zhi-Hong, Hiroko Miyahara, Jiro Takeo and Masashi Katayama. Diet High in Fat and Sucrose induces Rapid onset of Obesity-related Metabolic Syndrome partly through Rapid Response of Genes involved in Lipogenesis, Insulin Signalling and Inflammation in Mice, Diabetology and Metabolic Syndrome. 4.1 (2012): 32. Read More
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