Differences On Body And Tissue Weights

In the scientific method lab, I explored the different food options for mice in order to find the best one that will help them gain weight. To succeed in this lab, I needed to examine several types of foods including fruits, raw meat, cooked and uncooked foods. In this experiment I used cooked macaroni as a positive control and for the negative control I didn’t feed the mice any food, only water. The main objective of this study was to determine the best solution that will help me understand the metabolism of mice. All mice used in this study were given the same resources, but the only difference was the different types of foods fed to the mice to understand the changes of weight gain or loss between the mice.

Mediterranean diet, a low-carbohydrate, high protein diet, a vegan diet and a vegetarian diet all of which to have shown to improve metabolic conditions. The degree of the improvement varies from patient to patient therefore, it is necessary to evaluate each patient based on their only needs and individual metabolic demands. It is recommended that patients with pre-diabetes be made aware of beneficial nutrition intervention. Knowing what diet is best for the patient can significantly help with the risks of developing diabetes type 2. Medical nutrition therapy plays a role at three levels, primary prevention, secondary and tertiary prevention. For the purpose of this paper primary prevention is observed to help aim in delaying or arresting the development of diabetes. Different types of diet have been shown to be associated with improvement in metabolic condition. Modest weight loss has been shown to improve insulin resistance so either a low carbohydrate, low-fat calorie-resistance, or Mediterranean diet may be effective in the short term (Khazrai et al.,

Genetic research of obesity was partly successful in establishing obesity in model organisms – rodents where obesity occurs spontaneously together with other pathological aspects (insulin resistance, …). The main cause of monogenic obesity in these model organisms are common mutations always present in only one gene. Results of research on model organisms allowed us to understand biological mechanisms of calorie intake and regulation and maintenance of body weight. The most important insight into obesity was achieved in 1994 after discovery of ob gene encoding for leptin. In two years period, using screening method, candidate homologous genes, selected on genetic study basis on mice, another five genes were identified. Mutations on these genes were found to be the cause of autosomal recessive or dominant monogenic obesity. Products of these genes are leptin and its receptor, proopiomelanocortin (POMC) melanocortin receptor 4 (MC4R) and

In wild type mouse there is no effect on food intake, body weight and blood glucose though we give more leptin because here the leptin receptors are constant. But, in ob/ob mouse the food intake, body weight and blood glucose levels are decrease because the presence of leptin receptor. However, in the db/db mouse there is no effect due to the absence of the leptin

The current study demonstrates that diabetic group induces a decrease in body growth rate during the experimental period studied as compared to control group. The decrease in body weight in diabetic rats could be due to dehydration and catabolism of fats and proteins. Such results are in agreement with previous studies[ , ]. However, group III showed increase in body weight that renders them to near the normal control group. The increase in body weight of glibenclamide treated rats may be due to increase insulin secretion or increase food consumption. Also, oral administration of Ch.t extract for eight weeks to diabetic rats increased their food consumption and improved body weight. This could be due to a better control

In a study conducted in 1985 observing primates, it was determined that the major effect of dietary cholesterol is its LDL raising effects. High intakes of cholesterol increase the number of circulating LDL’s and it can also change its size and composition. [12] It was during this time period that the mechanisms by which SFA are thought to increase blood cholesterol concentrations came about. One mechanism for the increase in LDL cholesterol levels is the suppression of LDL receptor activity. Studies in tissue cultures have shown that increasing the cholesterol content of a cell will down-regulate synthesis of LDL receptors. [13] This will lead to an increase in concentration of blood cholesterol. Another cause for an increase in blood cholesterol concentration through intake of dietary SFA is the composition of the newly secreted lipoproteins. With a high saturated fat intake, the LDL’s become rich in cholesterol esters, leaving the triglycerides in the blood. [14] The use of non-human primates in

The goal of the study was to determine if mice liver samples with lower iron levels have an increased sensitivity to insulin resistance. Three objectives were tested in the study. First objective was to compare the control fat levels with the high fat levels according to their iron levels. Secondly, was to compare

Metoformin is a medication used to treat Type 2 diabetes. Metformin is classified as a biguanide and antidiabetic medication. Its therapeutic classification is an antihyperglycemic. Metformin, which is the drug’s generic name, is also known under its trade names: Fortamet, Glucophage, Glucophage XR, Glumetza and Riomet. Metformin is an oral hypoglycemic medication and has three main actions: Metofrmin increases the binding of insulin to insulin receptors in skeletal muscles and fat, which works to improve tissue sensitivity to insulin. Through this action, glucose is able to be transported into skeletal muscles and fat and the body is able to use glucose to function properly. Metformin also suppresses gluconeogenesis, which is the production of glucose from non-carbohydrate sources such as fat and protein. Metformin also prevents the liver from converting stored glycogen into glucose. All these actions work together to lower the level of blood sugar and also lower the Hemoglobin A1C value, ensuring diabetics have better control of their blood sugar.

This explained the low birth weight in undernourished rats but was rejected by Hardikar when he analysed potential single nucleotide polymorphism loci including methylenetetrahydrofolate reductase (mthfr) and discovered no genetic alterations. The thrifty genotype model also suggests an undernourished intrauterine environment is responsible for fetal programming that increases susceptibility to type - 2 diabetes in offspring. The second generation of recuperation rats should have demonstrated less susceptibility to type - 2 diabetes as they were well nourished during fetal development, but Hardikar discovered the undernourished and recuperation rats both demonstrated an increased susceptibility to streptozotocin induced diabetes that indicates type - 2 diabetes was not explained by low intrauterine

Insulin resistance can also be caused by increased triglycerides and free fatty acids intake. This is due to the effect Triglycerides and free fatty acids have on insulin stimulated signal pathways, translocation protein-4 and glucose uptake (Choi, Jung, Park, & Song, 2004). It is found that CLA has a regulatory effect on glucose and lipid metabolism regulators. CLA affects the PPAR-y ligand, a major receptor that influences the expression and transcription of genes that are related to the metabolic effects of glucose and lipids. Such protein regulators as aP2, insulin-dependent glucose transporter 4, FATp, ACS and adiponectin are all influenced by increased CLA. (Xiao-Rong Zhoua, Chang-Hao Suna, Jia-Ren Liua, b, Dan Zhaoa, 2008). It was also theorized that CLA may act on other glucose regulators such as phosphoenolpyruvate carboxylase, glucose-6-phosphate, glucokinase, sterol-regulation element finding protein, acyl coenzyme A oxidase, fatty acid synthase and uncoupling protein. Testing done on rats with a mixture of cis 9, trans 11 and trans 10, cis 12 CLA had found that the only effected regulatory agents were regulators involved in gluconeogenesis such as Phosphoenol carboxykinase and transcriptional factors, sterol-regulating element binding protein-1c and PPAR-y (Choi, Jung, Park, & Song, 2004). The main regulatory effect on insulin resistance was the effect on ligand PPAR-y, a key regulator in lipid homeostasis. Mixtures of CLA isomers consisting of cis 9, trans 11 and trans 10,cis 12 effect gene expression of PPARy mRNA in rats. It was found to have affected the levels of aP2, FATP, ACS and adipoenectin mRNA expression in adipose tissue. CLA increased These regulatory proteins resulting in an uptake of free fatty acids into the adipose tissue and decreasing uptake into the muscle tissue. This has been found to improve muscle insulin

L., Moreno Luna, A. Y., Reed, R. L., Miranda, C. L., Bobe, G., Proteau, R. R., & Stevens, J. F., 2013). The highest dose group had a notably lower plasma glucose level in comparison to the control group, in males but not females and there was also a large decrease in body weight for male rats in the highest dose group; In comparison to the rats that received no xanthohumol, which was also not seen in female rats either (Legette, L. L., Moreno Luna, A. Y., Reed, R. L., Miranda, C. L., Bobe, G., Proteau, R. R., & Stevens, J. F., 2013). One interesting thing researchers learned was that the plasma cholesterol, insulin, triglycerides, MCP-1(monocyte chemoattractant protein-1), as well as food intake were not affected by treatment. These findings prove that xanthohumol has beneficial effects on markers of metabolic syndrome. This is useful because this means that it has been proven that researchers have answered their thesis and discovered that xanthohumol does have an effect on lowering body weight in obese male Zucker fa/fa rats. With this knowledge I believe that if we continue to experiment with xanthohumol as a potential drug, we would be able to eventually learn how to apply it to humans safely, in the hopes of creating a new efficient treatment alternative or even a cure for

This primary article aimed to determine whether Wistar rats had a change in weight and food intake after consuming non- nutritive sweeteners and sucrose. 30 Wistar rats weighing about 200-300 g were taken for this experiment. They were kept in a 44 x 34 x 16 cm cage to control their activity, and divided into 3 groups of 10 Wistar rats, where each group was given either aspartame, sucrose or saccharin incorporated with yoghurt and water. This experiment was of 12 weeks, after which their body mass was measured. The final mass was determined by substracting the basal mass from the gained mass. It could be seen that the Wistar rats consuming aspartame and saccharin gained more weight compared to the Wistar rats feeding sucrose. It could be concluded

Figure 3 shows the percentage of gain in body mass compared to the initial mass of the body at the 6, 12, and 18-week time points. The vitamin D deficient groups showed the lowest percentage of body mass gain compared to the vitamin fed groups. Even though smoking was independent, and played no affect in body mass, the smoking vitamin D deficient mouse showed the lowest body mass gain at every single point.

Those on a Mediterranean-style diet are prone to have higher HDL, or “good” cholesterol levels, which help support heart health. Inuit Eskimos, who get plenty of Omega-3s from eating fatty fish, also tend to have increased HDL cholesterol and decreased triglycerides, or fats in the blood. Research studies have shown that fish oil supplements reduce triglyceride levels. Finally, walnuts (that contain high levels of alpha linolenic acid, or ALA, which is type of Omega-3 fatty acid) have been reported to lower total cholesterol and triglycerides in people who have high cholesterol levels.

Studies have been conducted on the pathogenesis of the Coronary heart disease and most of these studies have highlighted metabolism mechanism of fats. The studies have revealed that as there is a need to feed special diets to the patients with Coronary heart disease; these diets are to be designed in a way that the level of total blood lipid can be maintained within the healthier limits (Vlodaver, 2012, p. 45). It has been observed that if the daily intake of fat in the Coronary heart disease patients is limited to 50gm, than the maintenance of total bloody lipid levels can be assured.