Weight gain

metabolism needs further investigation. BAT is known to affect energy metabolism in murine models. Indeed, Lowell et al. showed that the ablation of BAT leads to obesity [ 13 ]. Feldmann et al. drew the same conclusion, showing that UCP1 ablation led to obesity in mice [ 14 ]. Studies using fluorine-18 fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET) scans have evi- denced the presence of BAT in adults [ 15 – 18 ]. 18 F-FDG is currently used in oncology to mark tumours but it is not specific and has been found in high glucose metab- olism organs such as BAT [ 19 – 21 ]. BAT is localized in the cervical and supraclavicular regions [ 22 , 23 ]. Only two studies, including ours, have focused on BAT activ- ity during breast cancer chemotherapy [ 24 , 25 ]. Rous- seau et al. studied BAT uptake variations among 33 early breast cancer patients who had 5 FDG PET scans during chemotherapy. The authors found that BAT up- take was highly variable across patients, independently from outdoor temperatures. They also showed that pa- tients treated with taxane-based chemotherapy were those with the more significant changes on PET-CT scan compared to those treated with anthracycline-based chemotherapy [ 25 ]. Our team hypothesised that chemo- therapy decreases BAT activity and leads to weight gain. Indeed, our previous pilot study on a small sample of pa- tients (26 early breast cancer patients included in the AVATAXHER trial in Jean PERRIN Comprehensive Cancer Centre) showed a decrease in 18 F-FDG uptake in

 In the case of Sit-Ups test as strength, physical quality where (Daniel N. Kulund, 1982) set that this test has been picked as a test of muscular endurance (Frank Galligan, ‎David White, 2001) our results confirm it has a strong positive correlation between methods and Fitness Body Health. Where our results are consistent with (Cissik, John, ‎Dawes, Jay 2015) that, comparison of strength with body weight, we can see that the heavier athlete produced more power because he or she had to move a greater mass. Logical thing that the woman must require much strength to lift his overweight case Condition experimental 2 in level of the fitness body health. Where the Recent research has shown that the loss of muscle power (the ability to produce force quickly) are due to the loss of muscle mass, which contributes to the overall decline in lean body mass (the mass of the body—muscles) not overweight (Kay A. Van Norman, 2010). Thing consisting with the judgment of Lopez LM (2013) and Chebet JJ (2015) [18] side effects of pills method are consistently in weight gain and fatigue. While our conditions experimental, line with confirmation of (Q. Ashiton Aston PHD, 2011) that the relationship between BMI and fitness varied among tests. Lower fitness in three items (sit-ups, jump, distance run) was evident in boys and girls with higher BMIs in each age group.

absolute insulin values nearly doubled across the weight change groups for both men and women (Table 2). These relationships remained highly significant even with adjustment for change in waist circumference (data not shown). Reported smoking, alcohol use, and sports activity showed similar frequencies across most weight change classes in men and women, except for those with marked weight gain (> 9 kg), who were more likely to be smokers, non-drinkers, and less active on univariate analyses (p<0.01 for each, data not shown). Therefore, we did additional models evaluating associated change in the individual syndrome parameters across weight change groups which also adjusted for self-reported frequency of daily smoking and alcohol use and weekly sports activities. Adjusted means for each of the metabolic syndrome parameters reported in Table 2 were unchanged after these adjustments (data not shown). We also did further analyses restricted to non-smokers and found similar results.

ble was BMI change per month: BMI adjusted for duration of study was chosen because of substantial variation in duration of trial participation between subjects. We identified all potential confounders for our GWAS by performing an extensive PubMed search using the search terms: antipsychotic-induced weight gain [AND] predictors [OR] association. We found age, sex, BMI at inception, and clinical improvement to be significantly associated with AiWG (Gebhardt et al., 2009; Raben et al., 2017). Age distri- bution was as would be expected of a first-episode psychosis cohort (Supplementary Figure 3). We did not correct for amisul- pride dose as amisulpride-induced weight gain was found not to be dose dependent (Nielsen et al., 2016; Pandit et al., 2019; Simon et al., 2009). Moreover, potentially weight influencing co-medica- tion did not influence BMI change significantly and was therefore not corrected for (Supplementary Figure 5). Thus, our association test was a linear regression with 14 covariates: age (years), sex (male vs female), BMI at trial inception, change (%) in total Positive and Negative Scale Score (PANSS), and 10 principal components to correct for genetic ancestry. During the course of writing, a new study we conducted found specific phenotypic variables associated with amisulpride-induced weight gain (Pandit et al., 2019), so a sensitivity analysis was run with these variables as covariates, namely, a diagnosis of major depression disorder (MDD) and employment status. Because of incomplete informa- tion on MDD, 11 subjects were excluded. This sensitivity model thus contained 15 covariates in 195 subjects: age (years), sex (male vs female), BMI at inception, MDD diagnosis (yes or no), employment (yes or no), and 10 principal components.

studying the relationships between metabolic parameters, gene expression, and histological observations, we were able to perform a comprehensive analysis of sc adipose tissue remodeling during the early phases of moderate weight gain in humans. We demonstrate that the initial events of adipose tissue development during a short period of positive energy balance in healthy men required the coordinated and time-dependent regulation of clusters of genes (Fig. 4). Inhibition of canonical Wnt signaling ap- pears to be an important step during adipose tissue re- modeling, which mostly includes coordinated neovas- cularization and extracellular matrix modifications. Additional factors, such as those related to the angiotensin system, apelin, or other growth factors may contribute to the correct orchestration of these interrelated processes to lead to an efficient storage of lipids and development of adipose tissue. These pathways therefore represent poten- tial targets to look after in pathologies of adipose devel- opment, including obesity.

The likely mechanism of increased weight gain in WD-fed PIF1 KO females was decreased locomotor activity. Both light and dark cycle activities were significantly reduced in PIF1 KO female mice after just four weeks of WD feeding when body weight differences were apparent, but modest. Additionally, there was a trend of decreased activity (25% reduction) after just two weeks of WD feeding prior to gross differences in body weight ( S1C Fig ). The importance of this two-week time point is that it was a weight-matched (pre-weight gain) cohort [ 41 ] that was evaluated pre- and post-WD exposure. Notably, when the activity trend is analyzed across all experiments and timepoints in the study, we find a statistically significant difference between WT and PIF1 during ( S1F Fig ). In the absence of pre-weight divergence hyperphagia ( S1E Fig ), the evidence best aligns with the conclusion that there is an interaction between PIF1 deficiency and Western diet that modulates locomotor activity to accelerate weight gain. By extension, we speculate that a PIF1 deficiency in humans might only cause obesity on West- ern diets.

To further examine the functions of TSK in regulating metabolism, com- plementary experiments were performed in TSK-overexpressing mice. Briefly, mice were infected with AAV serotype 8 (AAV8) coding for either a control green fluorescent protein (GFP) or a full-length TSK. As expected, we detected high levels of TSK in the plasma of mice injected with AAV8- TSK ( Figure 4 A). As observed in TSK-null mice, TSK overexpression did not affect the expression of thermogenic genes in BAT ( Figure 4 B). We did not observe any change in BAT weight or obvious differences in BAT morphology between AAV8-GFP and AAV8-TSK mice ( Figure 4 C and D). Moreover, we measured no difference in body temperature following TSK overexpression ( Figure 4 E). Consistent with these findings, we found no effect of TSK overexpression on body weight gain ( Figure 4 F). We next sought to define the impact of TSK overexpression on glucose homeo- stasis. As depicted in Figure 4 G and H, TSK overexpression did not have any impact on glucose tolerance and insulin sensitivity. Overall, these results indicate that TSK overexpression does not affect BAT activation, body weight, and glucose homeostasis in mice.

WEIGHT GAIN MECANISMS AFTER DEEP BRAIN STIMULATION OF THE SUBTHALAMIC NUCLEUS IN PARKINSON’S DISEASE PATIENTS INTRODUCTION : Deep brain stimulation (DBS) of the subthalamic nucleus (STN) improves parkinsonian symptoms and attenuate motor fluctuations, it allows antiparkinsonian medication reduction but one of the fequent adverse effect is an important weight gain.

4. Discussion 4.1. Principal Findings Our study found an association between GWG, birthweight, and neonatal fat mass, after adjustment for maternal obesity and gestational diabetes, and without finding significant collinearity between these factors in the multivariate model. This association seemed mainly due to third trimester weight gain. We also confirm that gestational diabetes is associated with neonatal fat mass and that it enhances the effect of third trimester weight gain on birthweight and fat mass. Our main result however, is that obesity has the greater impact on neonatal fat mass and that the association between maternal obesity and increased neonatal fat mass cannot be explained by a specific pattern of weight gain. Moreover, the effect of weight gain does not differ according to the sex of the newborn. Because neonatal fat mass is associated with increased cardio-metabolic risk in childhood and adolescence as well as in adulthood [ 16 ], our findings suggest that pre pregnancy maternal nutritional status should be optimized.

has led researchers to reconsider the impact of antibiotics that are associated with obesity particularly when administered in early infancy (Table 1). Glycopeptides, derived from bacteriocins secreted by bacteria of the Actinomycetales order, are antibiotics largely used in human medicine but linked with weight gain both in animals and humans. Indeed, avoparcin, originally isolated from Streptomyces candidus, was associated with weight gain in farm animals, 10 whereas vancomycin, which is isolated from Amycolatopsis orientalis, was associated with significant weight gain and acquired obesity in humans 11 in addition to increased adiposity in animals. 12 In vitro, glycopeptides affect mainly Gram-positive bacteria due to inhibitory activity against peptidoglycan synthesis. However, Pediococcous and Lactobacillus are not susceptible to glycopeptides, with the notable exception of the L. acidophilus group. Even if the susceptibility depends on the bacterial species within the same genus, treatment with oral vancomycin in humans has been associated with a decrease in Clostridium,

Weight change is, therefore, influenced by dietary intake and physical activity [ 8 – 13 ], but may also be affected by more distant determinants interacting with each other [ 8 , 14 – 17 ]. Individual sensory liking, such as liking for fat sensation, sweet and salty tastes, may be associated with body weight. Indeed, previous studies have shown a positive association between liking for fat sensation and body mass index (BMI) [ 18 , 19 ] and an increased risk of obesity [ 20 ], and this relationship was largely mediated by food intake. Indeed, subjects with high fat liking have higher fat intake and lower intake of nutrient-dense foods [ 21 ]. Regarding psychological characteristics such as cognitive restraint, studies have shown a positive association with BMI [ 22 , 23 ], but the relationship with weight gain is controversial [ 15 , 22 , 23 ], whereas recent dieting (i.e., to be on a diet plan recently) seems to predict subsequent weight gain [ 15 , 23 ]. Uncontrolled eating and emotional eating also appear to be associated with higher BMI [ 23 , 24 ]. Dietary intake may also explain these relationships; cognitive restraint is associated with higher vegetable intake and lower intake of French fries [ 25 ], whereas uncontrolled and emotional eating are associated with higher consumption of energy-dense foods [ 25 , 26 ]. More distant determinants, such as demographic characteristics (sex, age) and socioeconomic status might also influence weight status [ 17 , 27 , 28 ] through dietary intake. For example, higher socioeconomic status is associated with a better diet quality [ 29 – 31 ].

Attenuation of brown adipose tissue activity during chemotherapy treatment: a new mechanism of weight gain in breast cancer women? Emilie Gadéa, E. Thivat, C. Merlin, R. Paulon, F. Kwiatkowski, J.B Chadeyras, B. Coudert, Yves Boirie, Béatrice Morio, X. Durando

5. Conclusions In conclusion, the present results show the pertinence of measuring key metabolic parameters and behaviors in re- sponse to obesogenic diets in a young growing rat model on a continuous basis. This study demonstrates that at a very early stage, HFD alters key functions related to appetite, feeding behaviors, satiation, fat storage, physical activity, metabolism, and sleep. It suggests that energy-dense HFD could induce a vicious cycle that promotes higher calorie intake and sed- entary behaviors, two major risk factors for the development of obesity and ensuing metabolic dysfunctions. Further, the results presented herein imply the existence of a transitory state where young animals accumulate visceral adiposity while increases in weight gain are not yet detectable in response to hypercaloric intakes. However, this transitory state may only last between 2 and 4 weeks and could develop further into obesity. We anticipate that the results derived from the present study could be applied to elaborate novel interventions in nutrition and physical activity to circumvent obesity and ensuing metabolic dysfunctions at an early stage in human pediatric populations, thus opening up new avenues in human clinical and behavioral nutrition research.

Figure 5. Bcl-2 expression in CD11c + cells increases the Gr1 low monocyte proportion, insulin sensitivity and M2 ATM content in DIO conditions. (a) Blood monocyte levels characterized as in Figure 1 in irradiated C57Bl/6 mice recipients of WT (white histograms, n = 8) or transgenic CD11c-hBcl2 BM cells (gray histograms, n = 9) fed a HFD for 22 weeks. (b) Relative frequencies of Gr1 low and Gr1 high monocytes in mice described in a. (c) Histogram shows the ratio Gr1 low /Gr1 high monocytes in mice described in a –c. (d) Weight gain in irradiated C57Bl/6 mice transferred with Tg CD11c-hBcl2 BM cells (gray) or with WT BM cells (white). Mice fed a diet of 60% kcal from fat (n = 10 Tg CD11c-hBcl2 and 10 controls). Plasma glucose during GTT (e) and ITT (f) in mice described in d fed a HFD for 17 weeks and after 12 h fasting (n = 6/6). (g) ATM content in mice described in a. Characterization of ATMs based on the expression of Mgl1 and CD11c. Ratio of M2/M1 macrophages. (h) Levels of mRNA expression of functional M1 and M2 markers were evaluated by quantitative PCR in AT from mice described in a (n = 10 controls and 7 CD11c-hBcl2 transgenic mice). Relative mRNA expression of M1 and M2 genes was normalized to the average expression of two housekeeping genes (hypoxanthine guanine phosphoribosyl transferase and ribosomal protein S3). *P o0.05. **Po0.01. Data are expressed as means ± s.d.

Mechanisms of body weight gain in parkinsonian patients after subthalamic stimulation: Implication of changes in energy expenditure. International Congress of Parkinson’s Disease and Mov[r]

Fat mass vs body mass index in anticipation of aerobic capacity to monitor weight gain in sports women ©2019 Mohammed et al. Copyright: 24 Citation: Mohammed Z, Mohammed S, Mokkedes MI, et al. Fat mass vs body mass index in anticipation of aerobic capacity to monitor weight gain in sports women. MOJ Womens Health. 2019;8(1):22‒25. DOI: 10.15406/mojwh.2019.08.00204 relationships Vo2max & Height are the superior parameters predicting the levels of estimated vo2max (Table 2). Based on these results, we agree on one hand that further studies are needed to implement the actual findings associated with this hypothesis. In addition, we invite our metabolic physician to develop equation which takes the account of ranges for BMI in terms of the weight category 9 as new anthropometric equations to determine change in body Weight fat-free mass, total body water and body fat. 40

Decrease in αβ/γδ T-cell ratio is accompanied by a reduction in high-fat diet-induced weight gain, insulin resistance, and inflammation Gwenaëlle Le Menn, Brigitte Sibille, Joseph Murdaca, Anne-Sophie Rousseau, Raphaëlle Squillace, Bastien Vergoni, Mireille Cormont, Isabelle Niot, Paul

Citation: Mohammed Z, Mohammed S, Mokkedes MI, et al. Fat mass vs body mass index in anticipation of aerobic capacity to monitor weight gain in sports women. MOJ Womens Health. 2019;8(1):22‒25. DOI: 10.15406/mojwh.2019.08.00204 relationships Vo2max & Height are the superior parameters predicting the levels of estimated vo2max (Table 2). Based on these results, we agree on one hand that further studies are needed to implement the actual findings associated with this hypothesis. In addition, we invite our metabolic physician to develop equation which takes the

The search yielded 200 studies of which 118 were excluded because of probiotic or host group de finitions, study design or missing outcome data ( Fig. 1 ). 82 studies, involving 153 compari- sons, were included in the quantitative synthesis. Included human studies involved 15 double-blind randomized controlled trials and two open-labelled randomized trials ( Table 1 ). Included animal studies involved 14 studies on experimental models and 51 on farm animals. After exclusion of two studies with high risk of bias (weight signi ficantly different at baseline, open label design), LCPs were not associated with signi ficant weight change in human adults (SMD ¼ 0.18; 95%CI (0.43e0.79)), infants (SMD ¼ 0.004; 95%CI ( 0.20e0.21)), or preterm newborn infants (SMD ¼ 0.10; 95%CI ( 0.32e0.12)). Meta-analysis of all comparisons in healthy humans and animals (134 comparisons, overweight and VLWB newborns excluded) resulted in weight gain but signi ficant heterogeneity (SMD ¼ 0.15; 95%CI (0.12e0.18); p < 0.001; I 2 ¼ 85%)

significant for girls (Chou et al., 2005). In fact, this influence can be clearly seen as children are more likely to pick up items that are in “Mac Donald’s” packaging (Robinson et al., 2007). More generally, Cutler et al. (2003) and Bleich et al. (2008) argue that the increased calorie intake (i.e., eating habits) plays a major role in explaining current obesity rates. Importantly, weight gain prior to adulthood set the stage