The energy cost of performing 1 and 3 sets of strength-type (6-8 RM) and endurance-type (30-35 RM) bench press exercise was estimated by indirect calorimetry in 10 male college students. The total net energy cost of performing 3 sets of endurance-type resistive exercise (20.57 ± 1.86 kcal) was significantly (p-1) the strength-type exercise (2.35 ± 0.19) resulted in a significantly (p

Jean Mayer has postulated the presence of glucoreceptors located primarily in the ventromedial hypothalamic nuclei of the brain which are activated by glucose in the measure that they utilize it. According to Mayer, hunger occurs when glucose is not available for metabolic purposes and satiation supervenes when glucose is made available. Control of this mechanism rests with the glucoreceptors. These receptors are believed to be destroyed when an injection of the compound goldthioglucose is given to mice. These animals subsequently become obese and are found to have gold deposits and lesions in the ventromedial area and also in other parts of the brain. If the glucoreceptors are destroyed and cannot respond to the presence of glucose in the blood, it would be predicted that food intake would not change with the glucose level. The purpose of this investigation was to see if the food intake of goldthioglucose injected animals is affected by a glucose injection. One hundred and twenty mice were divided into four groups. One group, the controls, received no goldthioglucose. The other three groups received the following dosages: .5 mg. of goldthioglucose per gram of body weight, 1.0 mg. of goldthioglucose per gram of body weight and 1.3 mg. of goldthioglucose per gram of body weight. Fifty seven days after the goldthioglucose injection a training period began in which the mice were taught to consume their entire daily food intake during a 50 minute period. Then the experimental period began during which the animals were maintained on the 23 hour and 10 minute deprivation schedule. During this period the mice were given intraperitoneal injections of 60 mg. of glucose or normal saline on alternate days for ten days. The amount of food consumed in the 50 minutes beginning 15 minutes after the glucose or saline injection was determined. Food intake of the goldthioglucose injected animals was not different than that of the controls under any factor of the experiment. The results do not support Mayer's idea that the glucoreceptors as he describes them are destroyed by goldthioglucose.

Obesity is an urgent global public health concern as prevalence rates continue to increase, especially among children. At the cellular level obesity is defined by an increase in adipocyte number (hyperplasia) and size (hypertrophy). Both lead to the dysfunction of adipose tissue, which has been identified as the link between obesity and chronic disease. Bioactive compounds, naturally occurring in fruits and vegetables, hold enormous potential in regulating adipocyte biology. Quercetin, the most commonly consumed dietary flavonoid, is a strong potential anti-obesity agent that has been implicated as an AMP-activated protein kinase (AMPK) activator and shown to ameliorate symptoms of metabolic syndrome in vivo. Here we investigated quercetin’s effect on (1) adipogenesis, the process of increasing adipocyte number, and (2) metabolism of mature adipocytes. In 3T3-L1 preadipocytes, quercetin dose-dependently inhibited adipogenesis, as evidenced by decreased lipid accumulation and expression of adipogenic markers such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/ enhancer binding protein (C/EBP) α, adipocyte fatty acid binding protein 2 (aP2), and acetyl-CoA carboxylase (ACC) on mRNA and protein levels. This inhibitory effect was limited to the early stages of adipogenesis (0-36 hours), and quercetin treatment altered the normal expression pattern of cell cycle related genes Cyclin A and p27, indicating quercetin may inhibit adipogenesis through cell cycle events. We next investigated quercetin’s ability to activate AMPK and the metabolic pathways related to AMPK activation: lipolysis and b-oxidation. Quercetin increased phosphorylation of AMPK and its downstream target ACC. Further, quercetin treatment (100μM) increased free fatty acid content in the media through an AMPK-dependent mechanism. Quercetin up-regulated mRNA expression of uncoupling proteins 3 (UCP3) and peroxisome proliferator-activated receptor-gamma co-activator 1 alpha (PGC-1a), indicating that quercetin may induce mitochondrial oxidative pathways, also through an AMPK-dependent pathway. These findings suggest (1) quercetin inhibits adipogenesis through the regulation of early cell cycle events required for adipogenic differentiation, and (2) quercetin’s activation of AMPK induces lipolytic and oxidative pathways. Taken together, quercetin could be further developed as an anti-obesity agent because of its potential to inhibit both hyperplasia and hypertrophy in vitro.

INTRODUCTION: Previous studies have shown that mammalian expressed CTRP3 functions to lower blood glucose levels in transgenic mice. However, the production of mammalian expressed CTRP3 is expensive and can only yield up to 1mg/L of recombinant protein. On the contrary, bacterial expressed CTRP3 is relatively inexpensive and can theoretically produce 70mg of recombinant protein per L of bacteria. The purpose of this experiment is to see if functional CTRP3 protein can be produced effectively and economically using bacterial expression system. METHODS: The ctrp3 gene was inserted into a bacterial expression plasmid vector and transfected into Escherichia Coli (E. coli) bacterium to produce recombinant Polyhistidine-tagged-CTRP3 in the presence of L-Arabinose. Optimal expression parameters were then tested in the transfected bacteria. Optimal expression was confirmed by measurement of CTRP3 in through immunoblotting. RESULTS: Once optimal expression conditions were established, large amounts of CTRP3 were generated and purified by commercial HIS purification systems. Due to post-translation modification of CTRP3, it is unclear if the purified CTRP3 will be functional. The next step in the process is to optimize the purification protocol and test the functionality of the bacterial expressed CTRP3. Support or Funding Information This research was supported in part by National Institute on Alcohol Abuse and Alcoholism of the National Institutes of Health under Award Number R03AA023612 and East Tennessee State University Research Development Committee (E82262).

Inactivity reduces insulin action. Energy surplus causes similar reductions to insulin action. Unless energy intake is reduced to match low energy expenditure during inactivity, a concurrent energy surplus may account for the lower insulin action. This study evaluated the effect of inactivity (sitting) with and without energy surplus on insulin action. Fourteen young (26.1 ± 4.5 years (M ± SD)), lean (23.7 ± 7.1% fat), fit (VO 2peak = 49.1 ± 3.3 ml*kg -1 *min -1 ) men (n=7) and women (n=7) completed each of 3, 24-hour conditions: an active condition (i.e. high energy expenditure with energy intake matched to expenditure) = ACTIV; (2) reduced energy expenditure (inactivity) with no reduction in energy intake (i.e. energy surplus) = INACTIV; (3) inactivity with energy intake reduced to match low energy expenditure = INACTIV LO-CAL. Insulin action was measured during a glucose infusion the following morning. Data were analyzed using linear mixed-effects models with planned contrasts. Compared to ACTIV, insulin action, defined as whole-body rate of glucose disappearance ( R d ) scaled to steady-state plasma insulin, was reduced 39% in INACTIV ( p < 0.001) and by 18% in INACTIV LO-CAL ( p = 0.07). Insulin action was also higher in INACTIV LO-CAL compared to INACTIV ( p =0.04). These results suggest that 1 day of sitting elicits large reductions in insulin action. Energy surplus accounts for half of the decline in insulin action, suggesting other factors are involved in the metabolic response to inactivity.

Introduction: Gestational diabetes mellitus (GDM) is a metabolic disorder that has been defined as glucose intolerance that is first identified during pregnancy. The etiology of GDM is not yet fully understood, but there are several risk factors that appear to contribute to its development such as advanced age at pregnancy, family history of type 2 diabetes mellitus, and a previous history of GDM. The discovery of predictive GDM biomarkers has the potential to enable early GDM detection and lead to earlier diagnosis and preventative interventions. Objective: Perform metabolomics analysis on plasma samples collected at pre-conception and at 26-weeks gestation to investigate metabolic differences between participants of the gestational diabetes prevention (GDP) clinical trial who developed GDM and those who did not. Methods: Targeted metabolomics, comprised of primary metabolomics, biogenic amines, and lipidomics assays, was performed using UPLC-MS on plasma samples collected from a subset of 30 participants that completed the GDP study at preconception and 26 weeks gestation. The samples used for this analysis were from participants who developed GDM (n=19) and those who did not (n=11) in their pregnancy following their participation in the GDP study. Results: Multivariate analysis revealed indoxyl sulfate as significantly higher in the GDM group at both preconception and at 26 weeks gestation (VIP scores > 2.9). Preconception samples collected at the end of the GDP intervention study PC 38:0 was higher in the GDM group versus the non-GDM group (p < 0.05) whereas thymidine was lower in the GDM group (p < 0.05), in addition to numerous cell membrane lipids (VIP > 2.0). At 26 weeks gestation, D-glucuronic acid was higher in the GDM group versus the non-GDM group (p < 0.03), while LPE 22:6, SM 18:1 (22:4), PE 38:6, PE 40:6, PE 40:7, and PE (O-38:0) were lower in the GDM group (p < 0.04), in addition to numerous cell membrane lipids (VIP > 2.0). Discussion: The differences observed between the GDM and non-GDM groups at the two plasma collection time points may suggest metabolic alterations associated with GDM-induced metabolic dysregulation. These findings may help direct future research to focus on changes in lipid metabolism during pre-pregnancy for possible biomarkers of GDM. Repeat studies with diverse cohorts are needed to help identify a panel of metabolites that may serve as early biomarkers of GDM.

As the most widely consumed drug around the globe, there is a vast array of contradicting research available on caffeine. One of the most debated and researched topics on caffeine is its effect on the brain. Meanwhile, the data on the neurological condition of migraine has information scattered throughout countless research articles and experiments. Although neither migraine or caffeine are completely understood by the medical world, this analysis attempts to give a more coherent understanding of the relationship between the two. This is done by first understanding the known and theorized mechanisms of caffeine as well as the pathologies of migraine. Discussions on channelopathies, current migraine medications, and case studies will be presented. After much background research, we hypothesized that caffeine could excite neurons at physiological concentrations to the point of activation. This was tested by targeting the transcription factor cFos using immunocytochemistry in vitro. The protein cFos was identified due to its rapid translation—just 15 minutes after stimuli—to indicate activation. In addition to a control culture, three different caffeine concentrations were tested on the neurons: 50 micromoles— average plasma level after 1-2 cups of coffee consumption, 100 micromoles—average plasma level after 5-6 cups of coffee also believed to be the therapeutic amount to defend against neurological diseases such as Alzheimers Disease, and 250 micromoles—the average plasma level considered to be toxic in humans. Indeed, we saw a 53.8% increase in cFos expression in the neurons as 100 micromolar of caffeine was added and exposed to the cell cultures for 24 hours. In order to ensure the results obtained in this study were physiologically relevant in vivo, known toxic levels were tested for in vitro neurotoxicity. It was found in vitro that at the non toxic plasma concentrations of 50 micromolar and 100 micromolar of caffeine did not display cellular death as tested by Trypan Blue viability testing, Crystal Violet morphologies, and fleurojade immunochemistry that tests for degeneration. Each of these experiments identified a significant death increase as the toxic level of 250 micromoles of caffeine were utilized. This allowed us to theorize that the activation of neurons found in these experiments due to caffeine exposure would apply the same effect in vivo.

Non-alcoholic fatty liver disease (NAFLD) is a liver disorder linked to obesity that is rapidly increasing in incidence worldwide. It is a disorder that ranges in severity; from a benign condition of hepatic steatosis to a potentially deadly one resulting in cirrhosis and hepatocellular carcinoma. It is currently known that NAFLD is strongly associated with various aspects of metabolic syndrome: insulin resistance, elevated triglyceride levels, obesity, and type two diabetes mellitus. The multifactorial pathogenesis of NAFLD is still uncertain and closer attention is needed on the effect of one’s diet on NAFLD. In this study, we directly compare a westernized diet containing high levels of fat and fructose to a diet high in fat and containing cholate using mouse models in order to determine the role of each dietary factor in the incidence and severity of the different stages of NAFLD. We will evaluate the severity of hepatic steatosis and hepatocellular damage via hematoxylin and eosin (H&E) stained liver tissue and the severity of hepatic fibrosis via trichrome-stained liver tissue. Our hypothesis is that mice on the fructose-based diet are expected to have higher levels of hepatic steatosis and hepatocellular damage relative to mice on the cholate-based diet while mice on the cholate-based diet are expected to have higher levels of hepatic fibrosis relative to the fructose-based diet. The results of this study will aid in elucidating and strengthening the connection between one’s diet and the prevalence and severity of NAFLD.

Background: Macronutrients play a critical role within collegiate athletes’ performance and health, with carbohydrates providing most of the energy needs for most athletes. There is little research examining the macronutrient intake of healthy collegiate female athletes across sports. The aim of the present study was to compare macronutrient intakes of female collegiate athletes within different sports and compare their intakes to recommendations. Methods: An observational study was conducted to determine whether a sample of female collegiate athletes (n=26) consumed the IOC nutritional recommendations. Sports included within the study were soccer, basketball, volleyball, and cross-country. Athletes were asked to complete a 6-day food log over a 2-week span, which included 2 weekend days during their in-season training phase. The body composition of athletes was also recorded. Macronutrient and overall caloric intakes were then compared to the IOC recommendations. Results: Overall caloric and carbohydrate intake were significantly lower than the IOC recommendations. Carbohydrate intake was notably low within soccer players (2.92 ± 1.01 g/kg/day) and basketball players (1.61 ± 0.41 g/kg/day). Fat intakes were recorded significantly higher than the IOC recommendations of 15-20%. Athletes demonstrated a significantly higher protein intake than the IOC recommendations when measured in g (100.56 ± 24.01) and g/kg (1.65 ± 0.54). Conclusion: This study found that female soccer, basketball, and volleyball players do not consume adequate macronutrient intakes compared to the IOC recommendations. The current study is one of the first to demonstrate a cohort of female cross-country runners consuming the daily recommendations of both overall caloric intake and carbohydrate intakes during their in-season phase of training.

Alzheimer’s disease (AD) is the most common form of dementia and a growing disease burden that has seen pharmacological interventions primarily fail. Instead, it has been suggested that preventative measures such as a healthy diet may be the best way in preventing AD. Prebiotics are one such potential measure and are fermented into metabolites by the gut microbiota and acting as gut-brain axis components, beneficially impact the brain. However, the impact of prebiotics in AD prevention is unknown. Here we show that the prebiotic inulin increased multiple gut-brain axis components such as scyllo-inositol and short chain fatty acids in the gut, periphery, and in the case of scyllo-inositol, the brain. We found in E3FAD and E4FAD mice fed either a prebiotic or control diet for 4-months, that the consumption of the prebiotic inulin can beneficially alter the gut microbiota, modulate metabolic function, and dramatically increase scyllo-inositol in the brain. This suggests that the consumption of prebiotics can beneficially impact the brain by enhancing metabolism, helping to decrease AD risk factors.