Matching Items (25)
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 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.
ContributorsSmith, John Clark (Author) / Caplan, Michael (Thesis director) / Herman, Richard (Committee member) / Barrett, The Honors College (Contributor) / Harrington Bioengineering Program (Contributor)
Created2014-05
Description
Millions of Americans live with motor impairments resulting from a stroke and the best way to administer rehabilitative therapy to achieve recovery is not well understood. Adaptive mixed reality rehabilitation (AMRR) is a novel integration of motion capture technology and high-level media computing that provides precise kinematic measurements and engaging multimodal feedback for self-assessment during a therapeutic task. The AMRR system was evaluated in a small (N=3) cohort of stroke survivors to determine best practices for administering adaptive, media-based therapy. A proof of concept study followed, examining changes in clinical scale and kinematic performances among a group of stroke survivors who received either a month of AMRR therapy (N = 11) or matched dosing of traditional repetitive task therapy (N = 10). Both groups demonstrated statistically significant improvements in Wolf Motor Function Test and upper-extremity Fugl-Meyer Assessment scores, indicating increased function after the therapy. However, only participants who received AMRR therapy showed a consistent improvement in their kinematic measurements, including those measured in the trained reaching task (reaching to grasp a cone) and in an untrained reaching task (reaching to push a lighted button). These results suggest that that the AMRR system can be used as a therapy tool to enhance both functionality and reaching kinematics that quantify movement quality. Additionally, the AMRR concepts are currently being transitioned to a home-based training application. An inexpensive, easy-to-use, toolkit of tangible objects has been developed to sense, assess and provide feedback on hand function during different functional activities. These objects have been shown to accurately and consistently track hand function in people with unimpaired movements and will be tested with stroke survivors in the future.
ContributorsDuff, Margaret Rose (Author) / Rikakis, Thanassis (Thesis advisor) / He, Jiping (Thesis advisor) / Herman, Richard (Committee member) / Kleim, Jeffrey (Committee member) / Santos, Veronica (Committee member) / Towe, Bruce (Committee member) / Arizona State University (Publisher)
Created2012
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 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.
ContributorsRay, Tyler John (Author) / Caplan, Michael (Thesis director) / Herman, Richard (Committee member) / Towner, Kali (Committee member) / Barrett, The Honors College (Contributor) / Department of Chemistry and Biochemistry (Contributor) / W. P. Carey School of Business (Contributor) / School of Human Evolution and Social Change (Contributor)
Created2015-05
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 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.
ContributorsBrown, Cole Truman (Author) / Herman, Richard (Thesis director) / Towe, Bruce (Committee member) / Barrett, The Honors College (Contributor) / Harrington Bioengineering Program (Contributor)
Created2015-05
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 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.
ContributorsZuo, Connie Wanda (Author) / Washo-Krupps, Delon (Thesis director) / Deviche, Pierre (Committee member) / Herman, Richard (Committee member) / Barrett, The Honors College (Contributor) / Department of Chemistry and Biochemistry (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
As obesity continues to grow across the world, better understanding of the disease, treatments, and outcomes becomes increasingly important. Animal models used to study these aspects of obesity have 3 phases: experimental (EXP), caloric restriction (CR), and weight regain (WR). For this study an ad libitum high-fat diet (HFD) was used to induce hyperphagia and weight gain in Sprague-Dawley rats in the experimental period. Rats then transitioned to a chow (CH) diet and energy intake (EI; kcal/day) was reduced 40-60% during the caloric restriction period. In weight regain, rats were given chow ad libitum. This protocol was run 3 times, once every academic school year (2017-2018, 2018-2019, and 2019-2020). Sample sizes listed in the order of high fat (HF) rats then chow (CH) rats for each year were as follows: 2017-2018 (n=11, n=8), 2018-2019 (n=12, n=8), 2019-2020 (n=14, n=10). Analysis of energy intake was performed on the first week of the experimental phase and the first week of the weight regain phase. <br/><br/>HF EXP rats showed hyperphagic average daily EIs compared to CH EXP rats for all 3 years (p<0.01-0.0001). HF WR rats were similar to CH WR rats in all applicable years in terms of average daily EI. However, both HF WR and CH WR rats were hyperphagic. HFD caused hyperphagia to be highest at the beginning of the first week of EXP and then EI decreased significantly as days went by. However, in WR, hyperphagia (HF WR and CH WR) was flat throughout the week. Obesity prone (OP) rats during EXP had similar EI behavior to obesity resistant (OR) rats during EXP within the same year. During WR though, OP rats had significantly greater average daily EI (p<0.05-0.001) compared to WR OR rats within the same year for 2 out of the 3 years. <br/><br/>These results suggest that HFD induces hyperphagia during weight gain. In weight regain, where HFD is absent, HF rats and CH rats are both hyperphagic. This suggests that WR induces hyperphagia in both rat groups. WR also induces a greater increase in EI for OP rats compared to OR rats. Therefore, hyperphagia seems to be driven by 2 mechanisms (HFD and WR). The profiles of the responses are different however. HFD induces hyperphagia that decreases over the first week and the level of hyperphagia is similar between OP and OR rats. WR induces hyperphagia that remains stable in the first week and is more pronounced in OP rats compared to OR rats.
ContributorsDoan, Ben (Author) / Herman, Richard (Thesis director) / Molenaar, Sydney (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
Description
This study was conducted to observe the effects of varying diets on weight regain after caloric restriction. Touted as a potentially effective non-invasive treatment to obesity, caloric restriction uses the gradual decrease in caloric intake to aid in weight loss. However, once a patient is taken off caloric restriction, a marked regain of weight regain occurs, nullifying the weight loss from caloric restriction. To find ways to suppress this weight regain, this study observed the effects of four different diets: low-fat diet (chow), high-fat diet (HFD), 0.5% concentration menthol infused chow, and 1% concentration menthol infused chow. Over a span of 3 years, 43 male Sprague-Dawley rats were placed through a strict feeding protocol: 3 weeks of chow food (3.1 kcal/gram), 8 or 12 weeks of HFD (5.42 kcal/gram), and caloric restriction for 4 weeks. Separate data analysis was conducted for the year 2017-2018, due to a slightly different protocol when compared to 2018-2019 and 2019-2020.
In 2017-2018, the results showed that 0.5% menthol (n=4) suppressed weight gain more effectively than both the baseline chow diet (n=4, p=0.022) and the HFD (n=4, p=0.027). Again in 2018-2020, the 0.5% menthol (n=6) showed promising results, showing significant suppression of weight gain when compared to chow (n=13, p=0.022). Unfortunately, the difference in weight gain in 1% menthol (n=6) was inconclusive when comparing to both chow and HFD. Although 1% menthol was inconclusive in its efficacy in suppressing weight regain, the promising results on 0.5% menthol show that menthol has the potential to be an effective treatment to both prevent rapid weight gain and maintain weight loss from caloric restriction.
In 2017-2018, the results showed that 0.5% menthol (n=4) suppressed weight gain more effectively than both the baseline chow diet (n=4, p=0.022) and the HFD (n=4, p=0.027). Again in 2018-2020, the 0.5% menthol (n=6) showed promising results, showing significant suppression of weight gain when compared to chow (n=13, p=0.022). Unfortunately, the difference in weight gain in 1% menthol (n=6) was inconclusive when comparing to both chow and HFD. Although 1% menthol was inconclusive in its efficacy in suppressing weight regain, the promising results on 0.5% menthol show that menthol has the potential to be an effective treatment to both prevent rapid weight gain and maintain weight loss from caloric restriction.
ContributorsLee, Justin (Author) / Van Horn, Wade (Thesis director) / Baluch, Debra (Committee member) / Herman, Richard (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
Excessive weight gain, otherwise known as obesity, has become a pervasive medical condition throughout the world. Though caloric restriction (CR) results in weight reduction, this weight loss is often unsustainable in the long term. As such, the goal is to find a treatment that can maintain the results of restricted energy intake (EI). Studies have found that dietary menthol could be a possible treatment and preventative measure for excessive weight gain. While several studies have found that, as an agonist of TRPM8, dietary menthol increases the energy expenditure (EE) of the body without impacting EI, they have not studied the efficacy of dietary menthol in preventing weight regain (WR) following a period of CR. Methods used in this experiment include studying young Sprague-Dawley rats during 24-hour periods towards the end of the following three phases: (1) an experimental phase of 12 weeks, comprised of ad-libitum feeding of high fat diet (HFD) to 10 rats and chow diet to 4 rats, (2) a CR phase of 4-weeks with controlled feeding of the HFD rats with either a chow diet (n=4) or chow diet + 0.5% dietary menthol (n=6) and keeping the other rats on chow (n=4), and (3) a WR period of 4-weeks with ad libitum feeding of the same diets as in CR. EI and EE (via indirect calorimetry) were measured over 24-hour periods and were divided by the rat’s respective body weight (BW) on testing day to normalize the sample population. The energy gap (EG) was determined by subtracting EE from EI. The experimental and WR phase revealed a positive EG or energy balance (EI > EE) whereas CR yielded a negative EG or energy balance (EI
ContributorsWest, Kynzie Michelle (Author) / Herman, Richard (Thesis director) / Molenaar, Sydney (Committee member) / Johnsson, Kailin (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-12
Description
Preliminary studies indicate that the use of dietary menthol may prevent excessive weight gain through the activation of the transient receptor potential melastatin family member 8 (TRPM8) ion channel. It has also been expressed that elevation of the core temperature (Tc) inducing mild hyperthermia via an increase in ambient temperature aids in a marked reduction of the drive to eat and weight gain. While caloric restriction (CR) aims to treat obesity and secondary sicknesses, weight regain is a common result during long term weight maintenance. The goal of these studies was to evaluate and identify if the menthol and mild hyperthermia mechanisms could couple synergistically to reduce or abrogate weight gain. Ambient temperature (Ta) was increased incrementally to identify the threshold in which rodents display mild hyperthermia. Our initial attempts at hyperthermia induction failed because of limitations in the environmental chamber. These trials fail to note a threshold at which elevated Tc is sustained for any period of time. The data suggests an ambient temperature of 36-38 °C would be appropriate to induce a mild hyperthermia. A mild hyperthermia is described as the elevation of Tc 2-3 ° above the hypothalamic set point. To facilitate future hyperthermia studies, an environmental chamber was designed. A wine cooler was converted to withstand the desired temperatures, through the use of heat tape, a proportional controller, and a translucent Plexiglas custom fit door. Beyond leveraging temperature to regulate weight gain, dietary changes including a comparison between standard chow food, high fat diet, and menthol supplemented chow food treatment illustrate a strong likelihood of weight gain variability. In this pilot study, weight gain expression when given a diet supplemented with menthol (1%) showed no statistical significance relative to a high fat diet nor chow food, however, it revealed a trend of reduced weight gain. It is assumed the combination of supplemental menthol and mild hyperthermia induction will exacerbate their effects.
ContributorsJohnsson, Kailin Alexis (Author) / Van Horn, Wade (Thesis director) / Herman, Richard (Committee member) / Towe, Bruce (Committee member) / Sanford School of Social and Family Dynamics (Contributor) / School of Life Sciences (Contributor, Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
The prevalence of excessive weight gain (obesity) has steadily increased since about 1980. Excessive weight gain is associated with many comorbidities; thus, a successful treatment is needed. The most common form of non-surgical treatment for excessive weight gain is caloric restriction with the intent to reduce body weight by 10%. Though this treatment is successful at reducing body weight, it often fails at maintaining the weight loss. Dietary menthol has been suggested as a possible treatment for excessive weight gain and has produced promising results as a preventative method for excessive weight gain. Our studies aimed at reducing weight regain and maintaining caloric restriction by feeding male Sprague-Dawley rats 0.5% dietary menthol during a period of caloric restriction, aimed at reducing their body weight by 10%, following an experimental period where the rats were fed a high-fat diet (HFD) or low-fat diet (LFD). The effects of the dietary menthol were observed during the weight regain period following the caloric restriction period. Two studies were conducted, and both were unable to achieve a maintenance of weight loss following caloric restriction, although our first study was able to produce a delay in weight regain and did not show any evidence of increased thermogenesis in menthol-treated rats. Our findings differ from the findings of previous studies on dietary menthol which could possibly be due to species effects, differences in procedures, age effects, or effects of different fatty acid compositions. The contrasting results in our studies could be due to genetic differences between litters used or a difference in manufacturing of the menthol diet between studies. Given the partial response to menthol in the first study, it can be suggested that the concentration of 0.5% may be below the threshold of menthol sensitivity for some rats. Future research should focus on increasing the concentration of dietary menthol from 0.5% to 1%, since the current concentration did not yield a reduction in weight regain or maintenance of caloric restriction.
ContributorsRascon, Kasandra (Author) / Herman, Richard (Thesis director) / Sweazea, Karen (Committee member) / Kim, Minjoo (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05