Synthesis Of Ob/Ob Mutant Mouse

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.

Most diabetes research had been done on rodents up to that point, though they possess multiple differences from humans in

Although scientists have identified genes as being one of the factors contributing to obesity, knowing what specific genes involved would be helpful. The Friedman group decided to try and find those specific genes with a series of breeding experiments of mice. The genes were mapped out and the group found a 650-kilobase segment on mouse chromosome 6 to be responsible and named it the ob gene (for obese)(Marx). This means scientists have found a gene responsible for the obese mice which became an important step in finding treatment options for what is now looking like a complicated issue. The next question to answer was whether this gene was being produced in adipose (fat) tissue. This would help determine if the gene was responsible for creating the unneeded fat. The search paid off as one gene was found being

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

Being overweight significantly increases the chances of developing a common type of diabetes, type 2 diabetes. In humans, type 2 diabetes is a relative insulin deficiency that causes the cells in the body to develop a resistance to insulin. Insulin, a hormone produced in the pancreatic islet beta cells, helps move sugars into the cell that can later be used as fuel. The deficiency occurs when the functions of the beta cells are damaged. Insulin is unable to be detected because the insulin receptors are damaged from an overload of insulin already present in the pancreas. This causes the insulin to lose its ability to help clear the sugar from the body. A large amount of humans and felines are beginning to develop diabetes mellitus at a fast growing rate due to the body being unable to

you have the more resistance your cells become to insulin, but you don 't have to be overweight

During the study, 20 islets were studied from each case, and the focus was to measure B-cell volume, frequency, replication, and the ability for the endocrine ducts to produce new islet (Butler, et al. 2003). Based on the findings, there was an increase of B-cell in the obese population. “Obese humans with IFG and type 2 diabetes had a 40% (P < 0.05) and 63% (P < 0.01) deficit and lean cases of type 2 diabetes had a 41% deficit (P < 0.05) in relative β-cell volume compared with nondiabetic obese and lean cases, respectively” (Butler, et al. 2003).

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

Leptin is released through the arcuate nucleus and leptin helps to check the fat content of the body. If there is not enough fat, then our body gets the signal to be hungry and eat something. There are two types of appetite control neuron in the arcuate nucleus. They are NPY neurons and POMC neurons. NPY neurons can stimulate the appetite and reduce metabolism (Ceballos 2016). When the leptin level is high, this reducing metabolism process can be inhibited. These neurons can work as hunger neurons that can be stimulated by ghrelin. This peptide hormone is made by and released by the gut to increase appetite. During fasting, high concentration of ghrelin can strongly stimulate appetite and decrease suddenly when you eat something. NPY neurons inhibited by PYY3-36 to decrease appetite. PYY3-36 is released by intestinal cells. This small peptide level is increased after a meal to lower the appetite (satiety) signal (Ceballos 2016). This PYY3-36 acts on hypothalamic appetite control mechanism. PYY3-36 is very low in obese people, causing them to feel hungry and gain weight. The other type of appetite control neurons in arcuate nucleus is POMC neurons. These neurons can lower or inhibit appetite and increase the metabolism. They are also useful in acting as satiety

Elmquist & Flier (2004) investigated some recently discovered literature about the hormone leptin. This article attempted to synthesize some new documented research about how leptin contributes to the activity within the central nervous system. The purpose of this article is to identify the importance of this newly synthesized information and lead it to new discoveries by promoting several well founded research questions.

The results for the baseline metabolic rate were as expected. The metabolic rates of the Tx and the Hypox rat were lower than the metabolic rate of the normal rat. The Tx rat could not produce thyroxine because it had no thyroid gland. The Hypox rat could not produce TSH which stimulates the thyroid to produce thyroxin.

Leptin and ghrelin are internal intermediary that affect feeding and appetite. Ghrelin is secreted by the stomach adjust short-term appetitive control (i.e. to eat when the stomach is empty and to stop when the stomach is filled). Leptin is secreted by white adipose tissue to signal fat storage reserves in the body and mediates long-term appetitive controls (i.e. to eat less when fat storages are high and more when fat storages are low). It plays an efficient role in the regulation of energy balance and body weight by decreaing food intake and stimulating energy expenditure.39 Although, administration of leptin may be effective in a small subset of obese individuals who are leptin deficient. Most obese individuals are thought to be leptin resistant

Many studies have shown that high VF is significantly related to insulin resistance [11]. Normal weight individuals with low subcutaneous fat, but increased VF had greater insulin resistance than those with lower VF [8]. When evaluating this relationship in obese, metabolically at risk obese had more VF and greater insulin resistance than MHO [5]. On the other hand, subcutaneous fat seems to be associated with increased levels of leptin [11], a hormone secreted by adipose tissue that signals the amount of energy stores (fat mass) available in the body [12]. Leptin levels are positively correlated with FM [12], with obese individuals exhibiting high leptin concentrations [11]. Since obese individuals have an excess of body fat, high concentrations of leptin should decrease energy intake and increase energy expenditure which would promote a return to normal weight. Despite the potential physiological function, the role of leptin in energy expenditure is not completely understood. Research has demonstrated obese individuals to have high

Reactive hypoglycemia, a rare form of hypoglycemia, increases insulin levels after the consumption of excess carbohydrates, leading to a drop in blood glucose levels. This differs from conventional hypoglycemia where blood glucose drops several hours after a meal, but can easily be returned to normal by the consumption of food. Reactive hypoglycemia can cause fatigue, dizziness, shakiness, and in extreme cases, a coma. Although no effective treatments exist, glucagon, a peptide hormone derived from pancreatic alpha cells, seems to reduce symptoms. In the proposed experiment, the effectiveness of glucagon relative to a regimen of dietary control, exercise, and Acarbose will be tested on Zucker-diabetic-fatty (ZDF) rats (Rattus rattus). Three

A laboratory rat strain known as a Zucker rat. These rats are bred to be genetically prone to diabetes, the same metabolic disorder found among humans.