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Insulin Resistance in Rats Exposed to a High Fat Diet

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Type II diabetes is a serious, chronic metabolic disease that has serious impacts on both the health and quality of life in patients diagnosed with the disease. Type II diabetes is also a very prevalent disease both in the United

Type II diabetes is a serious, chronic metabolic disease that has serious impacts on both the health and quality of life in patients diagnosed with the disease. Type II diabetes is also a very prevalent disease both in the United States and around the world. There is still a lot that is unknown about Type II diabetes, and this study will aim to answer some of these questions. The question posed in this study is whether insulin resistance changes as a function of time after the start of a high fat diet. We hypothesized that peripheral insulin resistance would be observed in animals placed on a high fat diet; and peripheral insulin resistance would have a positive correlation with time. In order to test the hypotheses, four Sprague-Dawley male rats were placed on a high fat diet for 8 weeks, during which time they were subjected to three intraperitonal insulin tolerance tests ((NovoLogTM 1 U/kg). These three tests were conducted at baseline (week 1), week 4, and week 8 of the high fat diet. The test consisted of serially determining plasma glucose levels via a pin prick methodology, and exposing a droplet of blood to the test strip of a glucometer (ACCUCHEKTM, Roche Diagnostics). Two plasma glucose baselines were taken, and then every 15 minutes following insulin injection for one hour. Glucose disposal rates were then calculated by simply dividing the glucose levels at each time point by the baseline value, and multiplying by 100. Area under the curve data was calculated via definite integral. The area under the curve data was then subjected to a single analysis of variance (ANOVA), with a statistical significance threshold of p<0.05. The results of the study did not indicate the development of peripheral insulin resistance in the animals placed on a high fat diet. Insulin-mediated glucose disposal was about 50% at 30 minutes in all four animals, during all three testing periods. Furthermore, the ANOVA resulted in p=0.92, meaning that the data was not statistically significant. In conclusion, peripheral insulin resistance was not observed in the animals, meaning no determination could be made on the relation between time and insulin resistance.

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2017-05

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Blood Flow as a Biomarker for Diet Induced Thermogenesis

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Adaptive thermogenesis is an innate mechanism that assists the body in controlling its core temperature that can be stimulated in two ways: cold and diet. When adaptive thermogenesis is stimulated through diet, the metabolic rate of the body should increase

Adaptive thermogenesis is an innate mechanism that assists the body in controlling its core temperature that can be stimulated in two ways: cold and diet. When adaptive thermogenesis is stimulated through diet, the metabolic rate of the body should increase and the metabolic efficiency of the body should decrease. This activation should, theoretically, help to control weight gain. A protocol was developed to study four male Sprague-Dawley rats throughout a fourteen week period through the measurement of brown adipose tissue blood flow and brown adipose tissue, back, and abdomen temperatures to determine if diet induced thermogenesis existed and could be activated through norepinephrine. The sedative used to obtain blood flow measurements, ketamine, was discovered to induce a thermal response prior to the norepinephrine injection by mimicking the norepinephrine response in the sympathetic nervous system. This discovery altered the original protocol to exclude an injection of norepinephrine, as this injection would have no further thermal effect. It was found that ketamine sedation excited diet induced thermogenesis in periods of youth, low fat diet, and early high fat diet. The thermogenic capacity was found to be at a peak of 2.1 degrees Celsius during this time period. The data also suggested that the activation of diet induced thermogenesis decreased as the period of high fat diet increased, and by week 4 of the high fat diet, almost all evidence of diet induced thermogenesis was suppressed. This indicated that diet induced thermogenesis is time and diet dependent. Further investigation will need to be made to determine if prolonged high fat diet or age suppress diet induced thermogenesis.

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2016-12

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Hepatic inflammatory response following high fat diet in adolescent male Sprague-Dawley rats

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There has long been a link tied between obesity and such pathological conditions as nonalcoholic fatty liver disease and type two diabetes. Studies have shown that feeding rats a diet high in fat results in hepatic steatosis and steatohepatitis. Using

There has long been a link tied between obesity and such pathological conditions as nonalcoholic fatty liver disease and type two diabetes. Studies have shown that feeding rats a diet high in fat results in hepatic steatosis and steatohepatitis. Using a novel short term diet of six weeks with male adolescent Sprague-Dawley rats, our laboratory sought to investigate the early effects of high fat intake on the liver. Prior findings in our laboratory found that a high fat diet (HFD) leads to nonalcoholic fatty liver disease as well as other symptoms of metabolic syndrome. This study hypothesized that rats fed a 60% HFD for 6 weeks, unlike a high sucrose or standard chow diet, would have an elevated expression of pro-inflammatory cytokines associated with steatohepatitis. TNF-α, TLR4 and XBP1 were chosen for their link to hepatic inflammation. The results of this study found that contrary to the hypothesis, the high fat diet did not induce significant changes in the expression of any inflammatory marker in comparison to a high sucrose or control chow diet.

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2015-05

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The Effects of Diet on Glucose Metabolsim of Maturing Rats

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Background: Both puberty and diets composed of high levels of saturated fats have been shown to result in central adiposity, fasting hyperinsulinemia, insulin resistance and impaired glucose tolerance. While a significantly insulinogenic phenotypic change occurs in these two incidences, glucose

Background: Both puberty and diets composed of high levels of saturated fats have been shown to result in central adiposity, fasting hyperinsulinemia, insulin resistance and impaired glucose tolerance. While a significantly insulinogenic phenotypic change occurs in these two incidences, glucose homeostasis does not appear to be affected. Methods: Male, Sprague-dawley rats were fed diets consisting of CHOW or low fat (LF), High Fat Diet and High Fat Diet (HFD) with supplementary Canola Oil (Monounsaturated fat). These rats were given these diets at 4-5 weeks old and given intraperitoneal and oral glucose tolerance tests(IPGTT; OGTT) at 4 and 8 weeks to further understand glucose and insulin behavior under different treatments. (IPGTT: LF-n=14, HFD-n=16, HFD+CAN-n=12; OGTT: LF-n=8, HFD-n=8, HFD+CAN-n=6). Results: When comparing LF fed rats at 8 weeks with 4 week glucose challenge test, area under the curve (AUC) of glucose was 1.2 that of 4 weeks. At 8 weeks, HFD fed rats AUCg was much greater than LF fed rats under both IPGTT and OGTT. When supplemented with Canola oil, HFD fed rats AUC returned to LF data range. Despite the alleviating glucose homeostasis affects of Canola oil the AUC of insulin curve, which was elevated by HFD, remained high. Conclusion: HFD in maturing rats elevates fasting insulin levels, increases insulin resistance and lowers glucose homeostasis. When given a monounsaturated fatty acid (MUFA) supplement fasting hyperinsulinemia, and late hyperinsulinemia still occur though glucose homeostasis is regained. For OGTT HFD also induced late hyper c-peptide levels and compared to LF and HFD+CAN, a higher c-peptide level over time.

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2015-05

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Diet-Induced Thermogenesis as Measured by Exogenous Norepinephrine Injections in High Fat Diet - Fed Rats: A Pilot Study

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It is presently believed that brown adipose tissue (BAT) is an important tissue in the control of obesity because it has the propensity to increase energy expenditure. The purpose of this study was to attempt to quantify the thermogenesis of

It is presently believed that brown adipose tissue (BAT) is an important tissue in the control of obesity because it has the propensity to increase energy expenditure. The purpose of this study was to attempt to quantify the thermogenesis of BAT when four rats were exposed to a progression of low-fat to high-fat diet. Exogenous norepinephrine (NE) injections (dose of 0.25 mg/kg i.p.) were administered in order to elicit a temperature response, where increases in temperature indicate increased activity. Temperatures were measured via temperature sensing transponders that had been inserted at the following three sites: interscapular BAT (iBAT), the abdomen (core), and lower back (reference). Data showed increased BAT activity during acute (2-3 weeks) high fat diet (HFD) in comparison to low fat diet (LFD), but a moderate to marked decrease in BAT activity during chronic HFD (6-8 weeks) when compared to acute HFD. This suggests that while a HFD may initially stimulate BAT in the short-term, a long-term HFD diet may have negative effects on BAT activation.

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2016-12

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Persistence of Weight Gain, Energy Intake, and Feed Efficiency in a Rat Population Inclusive of Obesity Prone and Obesity Resistant Male Sprague-Dawley Rats with Controlled Environmental Factors

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Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been

Obesity has reached epidemic proportions all around the world, and it has doubled in prevalence in both adults and children in over 70 countries from 1980 to 2015 (Afshin et al., 2017). Excessive weight gain in this proportion has been shown to negatively affect human cognition, reward neurocircuitry, stress responsiveness, and quality of life (Morris et al., 2015). Obesity is an example of a complex interaction between the environment (i.e., high-fat diets) and heredity (i.e., polygenic patterns of inheritance). The overconsumption of a high-fat diet (HFD) is an environmental factor that commonly induces weight gain (Hariri & Thibault, 2010). Two dietary-induced phenotypes have been observed in rats as a bimodal distribution of weight gain: obesity-prone (OP) and obesity-resistant (OR). Levin et al. (1997) investigated male and female HFD-fed Sprague-Dawley rats designated as OR when their weight gains were less than the heaviest chow-fed controls, and OP when their weight gains were greater than the heaviest chow-fed controls. OP rats showed greater weight gain, similar energy intake (EI), and similar feed efficiency (FE) compared to OR rats. Pagliassotti et al. (1997) designated male HFD-fed Wistar rats as OP and OR based on upper and lower tertiles of weight gain. OP rats displayed greater weight gain and EI than OR rats. These investigations highlight a predicament regarding rodent research in obesity: independent variables such as rat age, gender, strain, distribution of dietary macronutrients, and fatty acid composition of HFD and chow vary considerably, making it challenging to generalize data. Our experiment utilized outbred male Sprague-Dawley rats (5-6 weeks) administered a chow diet (19% energy from fat; 3.1 kcal/g) and a lard-based HFD (60% energy from fat; 5.24 kcal/g) over eight weeks. Separate rat populations were examined over three consecutive years (2017-2020), and independent obesogenic environmental variables were controlled. We investigated the persistence of weight gain, EI, and FE in HFD-fed rats inclusive of a population of designated OP and OR rats based on tertiles of weight gain. We define persistence as being p > 0.05. We hypothesize that the profiles (periodic data) of the dependent variables (weight gain, EI, FE) will be similar and persistent throughout the three separate years, but the magnitudes (cumulative data) of the dependent variables will differ. Our findings demonstrate that HFD, OP, and OR groups were persistent for periodic and cumulative weight gain, along with FE across the three consecutive independent years. Our findings also demonstrate impersistence for periodic EI in all groups, along with impersistence in cumulative EI for CHOW, OP, and OR groups. Therefore, our results allude to an inconsistent relationship between EI and weight gain, indicating that EI does not completely explain weight gain. Thus, the weakness between EI and weight gain relationship may be attributed to a polygenic pattern of inheritance, possibly signaling a weight setpoint regardless of EI.

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2021-12