Mixed High-Fat and Stock Diet Caused a Greater Increase in Body Mass than High-Fat Diet Alone

Increased dietary palatability may lead to excess food consumption which in turn causes an excess of caloric intake and weight gain. Although most obesity studies in rodents utilize a high-fat diet, food variation, a combination of different diets for example, may actually increase body weight and fat mass beyond that of solely high-fat feeding. Purpose: To examine the changes in weight gain and body composition in mice that consume either a high-fat diet or a combination of high-fat and stock diet. Methods: 10 CD-1 male mice were randomly assigned to one of two groups based on dietary composition (N=5/group). HF mice consumed a high-fat diet (60% kcal from fat) and HF+Stock mice consumed a 50:50 combination of high-fat and stock diet (13.5% kcal from fat) for 24-weeks. Bi-weekly measurements were made on body composition (lean and fat mass) using an EchoMRI scanner and body weight using a digital scale. Food intake was recorded weekly. Results: HF and HF+Stock gained significant body weight, 41% and 66% respectively, from baseline to week 24 (P\u3c0.001, F12,84=45.483). On average, HF gained 23% lean mass (P\u3c0.001, F10,70=42.276) and 170% fat mass (P\u3c0.001, F10,70=31.873), while HF+Stock gained 27% lean mass and 260% fat mass from baseline. There were no differences between groups for body weight, lean mass, or fat mass. Conclusions: Although not significant, there was a greater increase in body weight, lean and fat mass in mice that consumed a combination of high-fat and stock diets. The results suggest diet variation has a positive effect in inducing obesity in mice. This study is limited in that only five animals were used in each group, thus leading us to believe that increasing the N per group will result in significant differences between groups. Expansion of this pilot study is warranted in the future

Consequences of Weight Cycling: An Increase in Disease Risk?

Research indicates that weight cycling, or “yo-yo dieting” is a common occurrence in obese populations. The long term negative health consequences of weight cycling are debated and it is unclear whether or not this weight change pattern poses a greater disease risk compared to obesity maintenance. This review discusses the prevalence of weight cycling and physiological alterations occurring during weight loss that promotes weight regain. We also discuss the effect weight regain has upon adipose tissue in terms of rate and type of accumulation. Also within this review are discussions surrounding the previously published literature based upon human and rodent research. We focus on previous limitations and difference in experimental design that have perhaps resulted in mixed findings concerning independent effects of weight cycling on health parameters. The final purpose of this review is to discuss future directions in evaluating the pro-inflammatory response to weight cycling in order to compare the disease risk compared to obesity maintenance

Foundations in Wisconsin: A Directory [32nd ed. 2013]

The 2013 edition of Foundations in Wisconsin marks the 32nd production of the print directory and the 13th year of the online version. The directory is designed as a research tool for grantseekers interested in locating information on private, corporate, and community foundations registered in Wisconsin. Each entry in this new edition has been updated or reviewed to provide the most current information available. Most of the data was drawn from IRS 990-PF tax returns filed by the foundations. Additional information was obtained from surveys, foundation websites, annual reports, and newsletters.https://epublications.marquette.edu/lib_fiw/1011/thumbnail.jp

Long-term Weight Gain in Response to High-fat Feeding in CD-1 mice

Background. Excessive weight gain is known to cause numerous health related consequences in humans and rodents. Due to ethical issues, it is not appropriate to cause weight gain in humans. From an experimental design prospective, murine models are often used to measure the effect of weight gain. Despite the validity of murine models, there is little published information concerning long-term weight gain when mice consume a high-fat (60% of calories from fat) diet. The purpose of this study was to examine weight gain during high-fat feeding in wild type CD-1 male mice. Methods. This study utilized data collected during the completion of four separate experiments. These experiments were selected so that we could compare: 1) the effects of husbandry type (i.e. individual vs. small groups), 2) weight gain following discontinuation of aerobic exercise training, and 3) the effect of changing to a high-fat diet following long-term acclimation to a stock diet. Two separate data sets were used for experiment 1 (N=120 and N=36). The data set used for experiment 2 demonstrates the long-term effects of the discontinuation of an exercise program (N=24). The data set for experiment 3 allows us to examine the effects of switching diets after an extended period of time (N=36). Change data was analyzed using separate linear mixed models (LMM) for weight gain and food intake. Results. Weight gain was similar over time between mice housed in groups or individually (experiment one). Following discontinuation of an aerobic exercise-training program, mice gained weight similar to that of sedentary controls that did not exercise (experiment two). When mice are switched to a high-fat diet at 25 weeks of age, they gain less weight than when they eat a high-fat diet at 6 weeks of age (experiment three). Conclusions. The results our investigation document long-term changes in mouse weight gain during ad libitum consumption of a high-fat diet. These findings will be useful to future researchers interested in using murine weight gain models

Monocyte and Cytokine Responses are improved by Baker’s Yeast β-Glucan Supplementation following Exercise in a Hot, Humid Environment

Strenuous exercise is known to suppress the immune system, which can increase the chances of getting sick in the hours after exercise. The purpose of this study was to determine if 10-d of supplementation with yeast b-glucan alters monocyte concentration, LPS-stimulated cytokine production, and plasma cytokine concentration in recreationally active subjects. Recreationally active subjects (29 men, 31 women, 22±4 y) completed 49±6 min of cycling (37±2°C, 45±5% relative humidity) after consuming either yeast b-glucan (250 mg/d, BG) or a placebo (sugar pill, PL) for 10-days prior to each exercise session. The investigators were blinded to the supplement conditions until all data was collected and analyzed. Venous blood was collected at baseline (prior to supplement), pre-, post-, and 2-hours (2H) post exercise. Total and subset monocyte concentration was measured by flow cytometry. LPS-stimulated production of 12 cytokines was measured using a whole blood assay. Plasma concentration of 13 cytokines was measured using a high-sensitivity MagPix assay. Monocyte (CD14+) concentration was significantly greater at 2H (P=0.05) with BG. Also, compared to PL, BG boosted LPS-stimulated production IL-2, IL-4, IL-5, and IFN-g at PRE and POST (P\u3c0.05). Plasma concentration of IL-2, IL-4, IL-5, IL-7, IL-10, and IFN-g were significantly greater at 2H in the BG compared to PL. In the placebo condition we observed the traditional response to strenuous exercise (rise at POST and suppression at 2H). It appears that 10-days of supplementation with BG primed blood leukocytes for the production of IL-2, IL-4, IL-5, and IFN-g. These cytokines were elevated prior to and immediately after exercise in LPS-stimulated cultures and subsequent elevation were observed at 2H with unstimulated plasma measures. In addition to cytokine changes, BG appeared to blunt post-exercise reduction in blood monocyte concentration, which may have implication of immune-surveillance. The key findings of the present study demonstrate that BG may be a suitable countermeasure to protect and boost the immune system following stressful exercise. Such boost is likely to lower the duration of the “open window” response. This study was funded by Biothera, The Immune Health Company

Leveraging Online Learning Resources to Teach Core Research Skills to Undergraduates at a Diverse Research University

Int J Exerc Sci 3(2) : 49-54, 2010. Today’s students have unique learning needs and lack knowledge of core research skills. In this program report, we describe an online approach that we developed to teach core research skills to freshman and sophomore undergraduates. Specifically, we used two undergraduate kinesiology (KIN) courses designed to target students throughout campus (KIN1304: Public Health Issues in Physical Activity and Obesity) and specifically kinesiology majors (KIN1252: Foundations of Kinesiology). Our program was developed and validated at the 2nd largest ethnically diverse research university in the United States, thus we believe that it would be effective in a variety of student populations

Voluntary Wheel Running during Weight Loss Leads to Differential Changes in Monocytes, Compared to Forced Treadmill Running

High-fat feeding and subsequent weight gain may contribute to innate immune dysfunction. Weight loss via calorie restriction and exercise represent one means to restore normal immune function. The purpose of the study was to examine how 8- weeks of aerobic exercise and low-fat diet affects weight gain, monocyte concentration, and monocyte cell-surface expression of TLR2, TLR4, CD80, and CD86. For 12- months, 24 male CD-1 mice underwent a pre-treatment phase, consuming either a low fat (10% fat) or high-fat (60% fat) diet ad libitum. Mice were randomly assigned to one of four groups (N=6/group): CN (low-fat sedentary), V-EX (voluntary wheel running), F10 EX (forced treadmill running), or SD (sedentary). V-EX, F-EX, and SD groups were switched from the high-fat to low-fat diet for an 8-week treatment period, while the CN group continued consuming the low-fat diet. Saphenous vein blood samples were analyzed using flow cytometry at baseline, week 4, and week 8. V-EX (36.4%) and F14 EX (27.1%) lost significant body weight over 8-weeks (P\u3c0.001). V-EX ran 4.4x more than F-EX (P\u3c0.001). As a group, V-EX had higher monocyte concentration than CN (48.9%) and F-EX (58.9%, P=0.004). Cell-surface expression of TLR2 (22.9%, P=0.002), TLR4 (33.3%, P\u3c0.001), and CD86 (18.6%, P\u3c0.001) increased from baseline to week 8. A time effect was seen in week 4 when CD80 expression was 42% greater for V-EX than SD (P=0.013). The present study confirms short-term exercise and low-fat diet consumption cause significant weight loss and altered immune profile as measured by increased TLR2, TLR4, CD80, and CD86 expression

Longitudinal, Diet-induced Weight Gain is Associated with Increased Blood Monocytes and Reduced TLR4 Expression

Excessive weight gain increases systemic inflammation resulting in increased disease risk. Toll-like receptor 4 (TLR4) reportedly mediates increases in inflammation; however, its role has not been fully evaluated. Objective. The purpose of this study was to determine the longitudinal effect of diet-induced weight gain on blood monocyte concentration and cell-surface TLR4 expression. Research Methods & Procedures. Male CD-1 mice were randomly assigned to high-fat (HF, n = 12) or low-fat (LF, n = 13) groups. Non-lethal, saphenous vein blood samples were collected at 0, 4, 8 and 12 weeks of treatment. Three-color flow cytometry was used to measure monocyte (CD11b+/CD14+) concentration and TLR4 cells-surface expression. Data were analyzed with a repeated measures ANOVA; significance was set at P\u3c0.05. Results. Body weight at week 12 was 21% greater in HF than LF (P\u3c0.05). At week 12 HF had 155% more monocytes (P\u3c0.05) with 24% less TLR4; Monocyte concentration and body weight at week 12 was negatively correlated with TLR4 gMFI (P\u3c0.05). Conclusions. The observed effects of high-fat feeding on blood monocytes are consistent with a phenotype, which may be associated with premature morbidity. The observed monocyte responses may be associated with immune dysfunction and diminished response to infection

Aerobic Exercise Training May Not Offset the Pro-inflammatory Effects of a High Fat Feeding

Aerobic Exercise Training May Not Offset the Pro-inflammatory Effects of a High Fat Feeding. Katie C. Carpenter, Lisa Esposito, Kelley A. Strohacker, Richard J. Simpson, Brian K. McFarlin. University of Houston, Houston, TX Increased adiposity is associated with an increase in systemic inflammation, which is involved in the pathophysiology of various disease states. A current hypothesis in our laboratory suggests that the toll-like receptor 4 (TLR4) pathway may link physical activity and systemic inflammation. PURPOSE: The primary purpose was to determine if 6-weeks of aerobic exercise training (5 days per week, 1 hour per day. 21-22m/min) would limit the increase in systemic inflammation resulting from high-fat (60% of calories from fat) feeding. A secondary purpose was to determine if changes in cell-surface TLR4 expression would account for observed differences in inflammatory status between mice which exercise and those that remain sedentary. METHODS: 36 CD-1 male mice were randomly assigned to one of three groups (N=12/group): HF (remained sedentary and consumed a high-fat chow (60% fat)), HF-EX (consumed the high-fat chow and underwent an aerobic exercise intervention (running 4.56±0.08 h/week for 6 weeks, or LF (sedentary and consumed a low-fat chow (10% fat)). Key outcome measurements were made on weekly saphenous vein blood samples (~40 uL) using 3-color flow cytometry. Blood glucose and cholesterol concentration were analyzed by an enzymatic assay. RESULTS: Absolute and percent body weight gain over 6-weeks was similar between HF and HF-EX, but significantly greater than LF (P\u3c0.001). HF and HF-EX had 66% more leukocytes than LF at weeks 3-5 (P\u3c0.0001). HF and HF-EX had 145% greater CD11b+/14+/TLR4+ cells than LF (P=0.001). There was no difference in the concentration of CD11b+ cells expressing IL-6 or TNF-alpha following LPS-stimulation between HF and HF-EX. No significant difference was found for blood glucose and cholesterol concentrations between groups. CONCLUSIONS: Exercise training did not prevent weight gain during 6-weeks of high fat feeding. Since HF and HF+EX gained a similar amount of weight, they did not differ with regarding to blood monocytes expressing TLR4. Both HF and HF+EX were elevated above LF. More research is needed to determine how changes in the blood relate to changes in peripheral tissue compartments

Exercise as a Prevention and Countermeasure to Diet-Induced Weight Gain

The purpose of this study was to evaluate the effectiveness of treadmill running at attenuating weight gain and immune dysfunction prior to or during a period of high-fat feeding in outbred CD-1 male mice. Mice were divided into four groups (N=10 mice/group): 4-weeks of treadmill running followed by 4-weeks sedentary (EX-SED), 4-weeks sedentary followed by 4 weeks of treadmill running (SEDEX), 8 weeks of treadmill running (EX), and 8 weeks sedentary (SED). After the first four weeks of the study, all groups began consumption of a high-fat diet to elicit a weight gain response. In order to track immune dysfunction, we measured peripheral blood monocytes and monocyte TLR4 expression at the conclusion of the study. We also completed a detailed analysis of body weight change over time. SED-EX was the only group that did not gain a significant amount of weight during the high-fat feeding. SED-EX had the lowest percentage of monocytes, as well as the highest total monocyte and classic subset cell surface TLR4 expression. EX and SED were not significantly different in any measurement. The present study demonstrates the importance of exercise training in counteracting the pro-inflammatory effects of diet-induced weight gain, as seen in SED-EX. Contrary to our hypothesis, exercise training prior to and throughout high-fat feeding did not prevent weight gain or attenuate the pro-inflammatory effects of weight gain. This could be due to an acclimation to the exercise intervention that blunted the anti-inflammatory effects of the exercise training during the high-fat feeding phase of the study. Similarly, exercise prior to high-fat feeding did not provide a lasting protective effect against the pro-inflammatory effects of diet-induced weight gain. Future research will endeavor to expand the current knowledge about monocyte subpopulations and to further elucidate the relationship between exercise and TLR4