Matching Items (22)

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Hyperinsulinemia

Description

Concurrent with the epidemic of childhood obesity (17% of adolescents), an unprecedented world-wide increase in the prevalence of several adiposity-related complications (including fatty liver disease (hepatic steatosis), type 2 diabetes

Concurrent with the epidemic of childhood obesity (17% of adolescents), an unprecedented world-wide increase in the prevalence of several adiposity-related complications (including fatty liver disease (hepatic steatosis), type 2 diabetes and early cardiovascular disorders) in this age group, has emerged. Two principle environmental variables play an essential role in the development and maintenance of obesity and in disturbing glucose homeostasis: a lack of physical exercise and overnutrition, i.e., high carbohydrate and high fat diets (HFD). It was our laboratory's intention to develop a rodent model to examine whether the metabolic instability observed in human pubertal children is also present in maturing rats and whether a HFD during this maturational period enhances adipose-related complications with or without an increase in body weight. We hypothesized that maturing Sprague-Dawley rats would reveal a profile of metabolic disturbances and that a disruption of the hyperbolic arrangement between insulin sensitivity and insulin release would be evident (statistically significant changes in fasting hyperinsulinemia, insulin resistance, and insulin release) indicating a high risk environment for future cardiometabolic diseases. It was observed that pubertal rats are metabolically impaired and that a HFD substantially enhances metabolic deficits with marked disturbance in insulin sensitivity (hyperinsulinemia). Additionally, substantial lipogenesis was observed in visceral and liver tissue, potentially as a result of hyperinsulinemia. Both phenotypes of maturing rats exposed to a HFD (obesity prone and obesity resistant) demonstrated "metabolic obesity" regardless of physical phenotype. These outcomes have relevance in the context of public health, particularly if lipocentricity is viewed as an essential element in the challenge of preventing and/or treating perturbations to the metabolic health of pubertal children.

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Date Created
  • 2014-05

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Drug Release from in \u2014 situ gelling material

Description

The main goal of this project was to study and understand the release of gentamicin from in – situ, self – reactive drug delivery gelling matrix. The motivation behind this

The main goal of this project was to study and understand the release of gentamicin from in – situ, self – reactive drug delivery gelling matrix. The motivation behind this was to create a drug delivery mechanism for gentamicin and eliminate the need for re–injecting the drug multiple times into the patient. Gentamicin is used to treat various different bacterial infections of the central nervous system, blood, kidneys, gall bladder, bile duct, heart cavity linings, and heart valves. Pentaerythritol–tetrakis
(3 – mercaptoproprionate; QT) was crosslinked with poly(ethylene glycol) diacrylate (PEGDA) having an average molecular weight of 575 with the help of Phosphate Buffer Saline (PBS), with a buffer ionic strength of 0.143M and a pH of 8.9 and 11, for the drug concentrations of 5 mg/mL and 50 mg/mL, respectively. The Michael – type reaction formed the crosslinked self – administering gelling matrix. With the gelling matrix starting to coagulate into a hydrophobic solid in about 5 minutes, the material was injected into Tygon tubing. After complete solidification, the drug – loaded gels were extracted from the tubing and divided into 1 cm cylinders. The cylinders with 5mg/mL and 50mg/mL drug concentration exhibited a sustained and controlled release curve for about 288 hours. This project as well as this drug delivery system can in the future be expanded for use in the delivery of more hydrophobic long – term drugs to the patient.

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Date Created
  • 2016-05

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

Description

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

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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Date Created
  • 2016-12

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Blood Flow as a Biomarker for Diet Induced Thermogenesis

Description

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

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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Date Created
  • 2016-12

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DOSE-RESPONSE CHARACTERISTICS OF ISOFLURANE ON PLASMA GLUCOSE CONCENTRATIONS

Description

Abstract: Purpose: The dose-dependent effects of isoflurane anesthesia on insulin inhibition and insulin resistance were compared in rats. Methods: Three rats were entered into the procedure with each rat being

Abstract: Purpose: The dose-dependent effects of isoflurane anesthesia on insulin inhibition and insulin resistance were compared in rats. Methods: Three rats were entered into the procedure with each rat being subjected to 3 different doses of steady state concentrations of isoflurane (1.75%, 2.0%, and 2.50%). A surgical plane of anesthesia was induced by continuous infusion of isoflurane via an induction box at 4.0% isoflurane and when anesthesia was achieved the infusion of anesthesia was lowered to the steady state concentrations of isoflurane. Plasma glucose concentrations were measured every 10 minutes until two or three consistent peak values were observed. After assurance of reaching peak values sub-cutaneous insulin (0.75 units/kg) was injected between the scapulas. Following the insulin injection plasma glucose concentrations were obtained every 10 minutes via pinprick until peak minimal glucose values were reached. If the plasma glucose of any animal reached a level approximately 50 mg/dL, subcutaneous glucose was injected (2.0 grams/kg) to prevent adverse effects of hypoglycemia. Results: For absolute plasma glucose post-anesthetic values a comparison of multiple mean glucose concentrations (single factor ANOVA) yielded p=8.06 x 10-6. A post-hoc analysis revealed significant p values between 3 pairs of means: 1.75%/2.0%= 0.004; 1.75%/2.5%= 0.03; 2.0%/2.5%= 0.02 . For normalized plasma glucose values post-anesthetic a comparison of multiple means (ANOVA) yielded a p value of 0.03. Post-hoc analysis indicated that the peak response was at 2.0% with significant difference between 1.75%/2.0% =0.03 and 2.0%/2.5%=0.02. There was no significance between glucose values 1.75%/2.50%=0.68. For plasma glucose values post-insulin both absolute and normalized a mean comparison analysis (ANOVA) concluded that during post insulin the data was not statistically significant as p=0.68. Conclusions: When absolute plasma glucose concentrations were normalized by the baseline taken at conscious state the dose-dependency disappeared and concluded the largest change in plasma glucose at 2.0%. Although the data post-insulin injection was not statistically significant it can be concluded that there was normal glucose uptake and that there was no impaired insulin action on the skeletal muscle.

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Date Created
  • 2015-05

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The Effects of Diet on Glucose Metabolsim of Maturing Rats

Description

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

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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Date Created
  • 2015-05

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Diet-induced alterations in energy homeostasis and central adiposity: liver and visceral adipose tissue

Description

There has been an alarming rise in the prevalence of obesity which has been attributed to the paralleled rise in consumption of high-fat foods. It’s commonly accepted that high-fat diets

There has been an alarming rise in the prevalence of obesity which has been attributed to the paralleled rise in consumption of high-fat foods. It’s commonly accepted that high-fat diets can lead to increased weight gain, however not all fats have the same physiological action. This study primarily focuses on the effect of canola oil, a monounsaturated fat, on energy homeostasis and body composition when it’s given as a supplement to a high-fat diet composed of saturated fatty acid. Rodent models were divided into three dietary groups: 1) low-fat diet (LFD), 2) high-fat diet (HFD) and 3) canola oils supplemented HFD (HF+CAN). After 4 weeks of dietary intervention, samples of epididymal fat, perinephric fat, and liver were analyzed across the three groups to see if the changes in energy homeostasis could be explained by the cellular behavior and composition of these tissues. Interestingly, the supplement of canola oil appeared to reverse the deleterious effects of a saturated fat diet, reverting energy intake, body weight gain and adipose tissue sizes to that (if not lower than that) of the LFD group. The only exception to this effect was the liver: the livers remained larger and fattier than those of the HFD. This occurrence is possibly due to a decrease in free fatty acid uptake in the adipose tissues—resulting in smaller adipose tissue sizes—and increased fatty acid uptake in the liver. The mechanism by which this occurs has yet to be elucidated and will be the primary focus of upcoming studies on the effect of monounsaturated fat on other diets.

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Date Created
  • 2015-05

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The Effects of a High-Fat Diet on Diet-Induced Thermogenesis in Cold-Stressed Rats: A Pilot Study

Description

Obesity is a rising problem in the country today, and countless efforts have been made to achieve long-term weight loss. Recent research indicates that through the manipulation of Brown Adipose

Obesity is a rising problem in the country today, and countless efforts have been made to achieve long-term weight loss. Recent research indicates that through the manipulation of Brown Adipose Tissue (BAT) activity within the body, weight loss can be achieved. The goal of this experiment was to understand the effects of a high-fat diet (HFD) on BAT activity and diet-induced thermogenesis in cold-stressed rats. It was predicted that the HFD would stimulate BAT activity and this would then drive up thermogenic activity to promote weight loss. Diet-induced thermogenesis was predicted to increase during the HFD phase of this experiment as the body would require more energy to digest the more calorically dense food. Upon arrival at six weeks of age, the rats were started on a low-fat diet (LFD) ad libitum for three weeks. They were then transitioned into a HFD ad libitum for the next 8 weeks. Throughout the experiment, the rats were maintained in a cold-stressed environment at 22°C. It was determined that one of the rats was identified as obesity prone, while the other three rats were obesity resistant based on the rate of weight gain and caloric intake. Obesity can decrease metabolism in the body for many reasons, yet it was not seen in this experiment that the obesity prone rat demonstrated decreased metabolism in comparison to the others. Based on the differences seen in the reference temperatures and the BAT temperatures, it was determined that the BAT was active throughout both the LFD and HFD phases. However, the BAT did not rise significantly during the HFD period as expected. More research is indicated with a larger sample size to determine if BAT activity does continue to increase during a HFD as a result of diet-induced thermogenesis.

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Date Created
  • 2016-12

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Insulin Resistance in Rats Exposed to a High Fat Diet

Description

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

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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Date Created
  • 2017-05

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Characterization of Food Intake and Weight Gain Responses in Rats on a High Fat Diet

Description

With the influence of the Western Diet, obesity has become a rising problem in the country today. Western Diet is characterized by the overconsumption of processed food that is low

With the influence of the Western Diet, obesity has become a rising problem in the country today. Western Diet is characterized by the overconsumption of processed food that is low in nutritional values and high in saturated fats. Study showed that every two out of three adults in the United States are either overweight or obese. Being obese increase the risk of many other disease such as diabetes, cardiovascular disease and insulin resistance. Besides being a great health concern, obesity is also cause a great financial burden. Many efforts have been made to understand the defense against obesity and weight loss. The goal of this study was to understand the characterization of food intake and weight gain responses when imposed on a high-fat diet (HFD) using rats. It was predicted that weight gain would be dependent on energy intake and it would have a significant effect on adiposity compared to energy intake. Data showed that energy intake had high significance with adiposity whereas weight gain showed no significance. Also for the rats that were on HFD, the obesity-prone (OP) rats exhibited a great amount of weight gain and energy intake while the obesity-resistance (OR) rats showed a similar weight gain to the controlled group on low-fat diet (LFD) despite being hyperphagic. This suggests that OR is characterized by equal weight gain despite hyperphagia but this alone cannot explain the boy defense against obesity. More research is needed with a larger sample size to understand weight gain responses in order to fight against the epidemic of obesity.

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Date Created
  • 2018-05