Body Fat Mass Levels Research Articles

Diets Differently Regulate Pulmonary Pathogenesis and Immune Signaling in Mice during Acute and Chronic Mycobacterium tuberculosis Infection.

Tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb) infection persists as a leading cause of mortality and morbidity globally, especially in developing and underdeveloped countries. The prevalence of TB-DM (diabetes mellitus) is higher in low- and middle-income countries where TB and DM are most prevalent. Epidemiological data suggest that slight obesity reduces the risk of TB, whereas DM increases the risk of pulmonary TB. Diets can alter the levels of body fat mass and body mass index by regulating systemic adiposity. Earlier, using a transgenic Mtb-infected murine model, we demonstrated that loss of body fat increased the risk of pulmonary bacterial load and pathology. In the present study, we investigated whether increased adiposity alters pulmonary pathology and bacterial load using C57BL/6 mice infected with HN878 Mtb strain and fed a medium-fat diet (MFD). We analyzed the effects of MFD on the lung during acute and chronic infections by comparing the results to those obtained with infected mice fed a regular diet (RD). Histological and biochemical analyses demonstrated that MFD reduces bacterial burden by increasing the activation of immune cells in the lungs during acute infection and reduces necrosis in the lungs during chronic infection by decreasing lipid accumulation. Our data suggest that slight adiposity likely protects the host during active TB infection by regulating immune and metabolic conditions in the lungs.

Serum adipocyte fatty acid-binding protein level is positively associated with aortic stiffness in nondialysis chronic kidney disease patients: A cross-sectional study.

Aortic stiffness (AS) is a major predictor of cardiovascular disease and mortality in patients with chronic kidney disease (CKD) and adipocyte fatty acid-binding protein (A-FABP) is a novel adipokine that is positively correlated with AS in the general population. Therefore, we investigated the correlation between serum A-FABP levels and AS in nondialysis CKD patients.Fasting blood samples and baseline characteristics were obtained in 270 patients with nondialysis CKD. Serum A-FABP concentrations were determined by enzyme immunoassay and carotid–femoral pulse wave velocity (cfPWV) measurements were acquired using a validated tonometry system. Patients with cfPWV >10 m/s formed the AS group, while those with values ≤10 m/s comprised the comparison group.Among 270 CKD patients, 92 patients (34.1%) were in the AS group. Compared to those in the comparison group, patients in the AS group were older (P < .001), had a higher prevalence of diabetes, along with higher serum A-FABP level (P < .001), larger waist circumference (P = .004), and lower estimated glomerular filtration rate (P = .001) but higher levels of body fat mass (P = .010), systolic blood pressure (P < .001), fasting glucose (P = .014), blood urea nitrogen (P = .009), and serum creatinine (P = .004). The serum log-A-FABP level was positively associated with log-cfPWV (β = 0.178, P = .001) in nondialysis CKD patients and multivariable logistic regression analysis identified serum A-FABP (P = .006), age (P = .001), and systolic blood pressure (P = .015) as independent predictors of AS in nondialysis-dependent CKD patients.Elevated A-FABP levels may be a significant predictor of AS in nondialysis CKD patients.

Вплив різних за структурою навантажень силового фітнесу на характер зміни морфометричних показників у жінок другого періоду зрілого віку

The purpose of the work was to study the features of the influence of power fitness programs different in structure and intensity on the morphometric parameters of the body of women of the second period of adulthood. Materials and methods. We examined 50 women aged 36 to 55 years (the second period of adulthood) who had no contraindications for health reasons to power fitness training. To achieve this purpose, the study participants were divided into 2 research groups (A and B), 25 people each. Each of the groups used the proposed program of power fitness training. Anthropometry and bioimpedancemetry methods were used in the course of the 3-month study to determine the peculiarities of the dynamics of morphometric parameters of the body of women of both groups under conditions of muscular activity of different orientation. Results and discussion. In the process of developing an experimental program of power fitness training for women of the second period of adulthood, mainly the whole training management mechanism was aimed at correcting the parameters of intensity of physical activity, which may allow to maximize the energy potential of the body and the level of functionality in general. Thus, the regulation of the value of load intensity was performed due to the following factors: the level of muscle tension was changed by reducing or increasing the duration of the concentric and eccentric phases of movement; the technique of performing the exercise was partially changed due to the amplitude and position of the body in space; the duration of rest intervals between sets was adjusted; the level of complexity of training exercises complexes and their variability was changed. The use of a generally recognized training program in power fitness, which is based on a set of physical exercises on training devices, helps to reduce the parameters of the circumferential body dimensions of women of the second period of adulthood (group A) by an average of 2.7% (p &lt;0.05). A corresponding tendency towards changes, but with less progression, was revealed when monitoring similar indicators of women in group B. The results of bioimpedancemetry, especially during the second and third months of training, show a decrease by 1.4% (p &lt;0.05) in the indicator of body fat mass in women of group B who in the process of doing fitness used the complex of innovative exercises with own body weight. However, in another group of women, we observe an almost imperceptible tendency towards a decrease in the controlled indicator by 0.2% during two months of power fitness training. A corresponding positive tendency towards changes was revealed in the process of step-by-step control over the indicators of active cell body mass in women of both research groups. Conclusion. The results obtained during the course of research prove that even an anaerobic load under the conditions of using a complex of innovative means of power fitness developed on the basis of exercises with one’s own body weight, but with corresponding changes of kinematic, dynamic and rhythmic characteristics of performance technique contributes to the positive dynamics of morphometric indicators almost in the same range as the load of aerobic orientation when using a generally recognized training program in power fitness with a set of exercises on training devices. At the same time, it was found that under the conditions of using the experimental training program, the level of body fat mass shows the most pronounced tendency towards decrease, regardless of age peculiarities

Особливості ендокринного статусу в дітей з ожирінням та поліморфізмами гена лактази

Актуальність. Ожиріння — це дисбаланс імуноцитокінової та нейроендокринної регуляції енергетичного обміну з надлишковим накопиченням жирової тканини в організмі, пов’язаний з формуванням хронічної прозапальної імунної відповіді, асоційованої з генотипом С/С 13910 гена лактази. Мета дослідження: визначити особливості тиреоїдного, статевого гормонального статусу, жирового обміну та формування лептинорезистентності в дітей з ожирінням та поліморфізмами (SNP) гена лактази (LCT). Матеріали та методи. Проведено комплексне обстеження згідно з діючим протоколом зі спеціальності «дитяча ендокринологія» 76 дітей віком 6–18 років з ожирінням та SNP LCT. Першу групу (n = 36) становили діти з генотипом С/С 13910, що асоціюється з лактазною недостатністю дорослого типу. До другої групи (n = 40) увійшли фенотипово схожі діти з генотипами С/Т та Т/Т 13910, що асоціюються з лактазною персистенцією. Визначення порушень жирового обміну проводили методом біоімпедансометрії на електронних вагах Tefal Bodysignal (Франція). Дослідження ендокринного статусу виконували за допомогою імунохімічного методу тестування з електрохемілюмінісцентною детекцією (ECLIA), генотипування гену лактази — за допомогою полімеразної ланцюгової реакції в режимі реального часу. Результати. У дітей з генотипом С/С 13910 виявляються статистично значимі відмінності в ендокринному статусі, пов’язані з підвищенням інсулінорезистентності у хлопчиків до 6,79 ± 1,12 за індексом НОМА проти 3,29 ± 0,99 у хлопчиків з генотипами С/Т та Т/Т 13910 при р = 0,028. У дівчаток з генотипом С/С 13910 відмічається відносне, в межах фізіологічної норми, зниження вільного естрадіолу до 40,10 ± 0,05 пг/мл порівняно з рівнем у дівчаток з генотипами С/Т та Т/Т 13910 — 75,61 ± 4,6 пг/мл при р &lt; 0,01, з одночасним патологічним підвищенням в 3,5 раза дегідроепіандростерону сульфату у віці 15–18 років до 594,50 ± 8,81 мкг/дл відносно рівня у дівчаток з генотипами С/Т та Т/Т 13910 — 167,06 ± 12,80 мкг/дл при р &lt; 0,01. Для дівчаток з генотипом С/С 13910 характерне статистично значиме (р &lt; 0,05) підвищення рівня лептину до 47,84 ± 4,40 нг/мл порівняно з дівчатками з генотипами С/Т та Т/Т 13910 — 32,54 ± 4,30 нг/мл. Порушення жирового обміну асоціюються з більш високим рівнем жирової маси тіла (ЖМТ) у хлопчиків та дівчат з генотипом С/С 13910 відносно дітей з генотипами С/Т та Т/Т 13910, а саме: у хлопчиків з генотипом С/С 13910 середній рівень ЖМТ становив 35,46 ± 2,52 %, тоді як у хлопчиків з генотипами С/Т та Т/Т 13910 — 25,04 ± 2,14 %. У дівчаток з генотипом С/С 13910 середній рівень ЖМТ становив 38,19 ± 2,25 %, тоді як у дівчат з генотипами С/T та Т/Т 13910 середній рівень ЖМТ — 28,99 ± 0,76 % при р &lt; 0,001. Висновки. Фактором ризику ожиріння в дітей є генотип С/С 13910 гена лактази, що асоціюється з лактазною недостатністю дорослого типу. Хлопчики 6–18 років, хворі на ожиріння, носії даного генотипу, мають в 1,5 раза вищий ризик формування інсулінорезистентності. Дівчата 15–18 років з генотипом С/С 13910, хворі на ожиріння, мають в 1,5 раза вищий ризик виникнення лептинорезистентності та в 3,5 раза вищий ризик інвертованого перебігу пубертатного періоду за рахунок гіперандрогенії надниркового генезу.

Levels of Physical Activity and Their Relationship With Motivational Determinants, Self-Regulation, and Other Health-Related Parameters in University Students.

Motivational processes and emotional self-regulation are relevant factors for predicting the practice of physical exercise and for certain health-related parameters. The aim of the present work, developed along two different phases, was, on the one hand, to determine the prevalence of physical inactivity and, on the other hand, to carry out a comparative analysis between physically active and inactive university students in relation to their motivational determinants, emotional self-regulation, physical condition, health-related quality of life and other health parameters. The results obtained showed a prevalence of physical inactivity of 12.78%. Physically inactive participants showed significantly lower scores in intrinsic motivation, emotion regulation, and in some dimensions of health-related quality of life, as well as significantly high levels of body fat mass. Lastly, logistic regression analysis identified low scores in Emotional Clarity (p= .009) and Identified Regulation (p = .011), and high scores in Amotivation (p = .006) as reliable predictors of a physically inactive lifestyle. These results are useful for the design and implementation of programs aimed at promoting health and physical activity, with special attention on physically inactive youth populations.

From famine to therapeutic weight loss: Hunger, psychological responses, and energy balance-related behaviors.

Understanding physiological and behavioral responses to energy imbalances is important for the management of overweight/obesity and undernutrition. Changes in body composition and physiological functions associated with energy imbalances provide the structural and functional context in which to consider psychological and behavioral responses. Compensatory changes in physiology and behavior are more pronounced in response to negative than positive energy balances. The physiological and psychological impact of weight loss (WL) occur on a continuum determined by (i) the degree of energy deficit (ED), (ii) its duration, (iii) body composition at the onset of the energy deficit, and (iv) the psychosocial environment in which it occurs. Therapeutic WL and famine/semistarvation both involve prolonged EDs, which are sometimes similar in magnitude. The key differences are that (i) the body mass index (BMI) of most famine victims is lower at the onset of the ED, (ii) therapeutic WL is intentional and (iii) famines are typically longer in duration (partly due to the voluntary nature of therapeutic WL and disengagement with WL interventions). The changes in psychological outcomes, motivation to eat, and energy intake in therapeutic WL are often modest (bearing in mind the nature of the measures used) and can be difficult to detect but are quantitatively significant over time. As WL progresses, these changes become more marked. It appears that extensive WL beyond 10%-20% in lean individuals has profound effects on body composition and physiological function. At this level of WL, there is a marked erosion of psychological functioning, which appears to run in parallel to WL. Psychological resources dwindle and become increasingly focused on alleviating escalating hunger and food seeking behavior. Functional changes in fat-free mass, characterized by catabolism of skeletal muscle and organs may be involved in the drive to eat associated with semistarvation. Higher levels of body fat mass may act as a buffer to protect fat-free mass, functional integrity and limit compensatory changes in energy balance behaviors. The increase in appetite that accompanies therapeutic WL appears to be very different to the intense and all-consuming drive to eat that occurs during prolonged semistarvation. The mechanisms may also differ but are not well understood, and longitudinal comparisons of the relationship between body structure, function, and behavior in response to differing EDs in those with higher and lower BMIs are currently lacking.

Hypothalamic inflammation: marker or mechanism of obesity pathogenesis?

Obesity and its associated metabolic and cardiovascular disorders are among the most challenging health problems confronting developed countries. Not only is obesity remarkably common, affecting more than one-third of U.S. adults, and very challenging to treat, but it is also tightly linked to type 2 diabetes and related metabolic disorders. A major obstacle to effective obesity treatment is that lost weight tends to be regained over time (1). Although the mechanisms underlying recovery of lost weight are incompletely understood, a large literature suggests that body fat stores are subject to homeostatic regulation, and that this process occurs in obese as well as normal-weight individuals. From this perspective, obesity can be viewed as a disorder in which the biologically defended level of body fat mass is increased. Recent findings implicate inflammation in key hypothalamic areas for body weight control in this process. In this review, we present an overview of energy homeostasis—the biological process that underlies the control of body fat mass—and describe evidence that defects in this regulatory system contribute to obesity pathogenesis. We then address molecular characteristics of hypothalamic inflammation and their implications for obesity pathogenesis (detailed more extensively in refs. 2,3), followed by evidence linking high-fat diet (HFD) feeding to neuropathological alteration of key hypothalamic areas controlling energy balance. We conclude by considering how cell-cell interactions may contribute to this deleterious hypothalamic response and the implications of these interactions for obesity pathogenesis. ### Homeostatic response to weight loss. Following a period of caloric restriction, lost weight is gradually but inexorably recovered in most individuals. This effect involves the capacity of the brain to sense the reduction of body energy stores and activate responses to compensate for this deficit. In simple terms, voluntary weight loss triggers increases of both appetite and energy efficiency, such that both sides of the energy balance equation shift …

Comparing estimates of body fat in children using published bioelectrical impedance analysis equations

The level of body fat mass (BFM) in childhood that is associated with weight related morbidity is unclear. Bioelectrical impedance analysis (BIA) offers an inexpensive, acceptable and portable method for measuring body composition in children. However, different equations have been derived to estimate BFM, and relationships between equations have not been explored. To compare body mass index (BMI) and BIA as tools for estimating adiposity-related health risks in children. Height, weight and BIA were measured in a population based cross-sectional survey of 341 healthy 5-year-old Australian children. Percent BFM was estimated using four published BIA-based predictive equations for pre-school children. Ranking of children according to total BFM was compared for all equations. Each equation produced different estimates of percent BFM. In general, increasing BMI was associated with increasing BFM, but wide ranges of BFM estimates were produced for children of similar BMI. For all of the equations, females had a higher percent BFM compared with males of the same BMI (p<0.001). Percent BFM estimates rose rapidly in children classified as overweight/obese (1990 UK growth standard). The equations were highly correlated in their ranking of children from lowest to highest percent BFM. Results support concerns about the validity of BMI as an accurate measure of absolute BFM. Percent BFM estimates produced by the four BIA equations were highly correlated, indicating they rank children according to BFM in the same order. This suggests any single equation could provide a measure of relative BFM in children for population and longitudinal studies.

Rebound Weight Gain as Associated With High Plasma Norepinephrine Levels That Are Mediated Through Polymorphisms in the β2-Adrenoceptor

A successful weight loss program is essential treatment for obesity-related diseases, but it is well known that the majority of individuals do not succeed in weight loss maintenance. The present study evaluates hormonal mechanisms and the relationship of beta2-adrenoceptor polymorphisms involved in individuals who regain weight after initially successful weight loss. Overweight Japanese men (n = 154) were enrolled in a 24-month weight loss program. Body mass index (BMI), total body fat mass, plasma norepinephrine (NE) and leptin levels, and beta2-adrenoceptor polymorphisms (Arg16Gly, Gln27Glu) were measured every 6 months for the 24-month period. Maintenance of weight loss was defined as significant weight loss (>or=10% reduction) from entry weight at 6 months and maintenance of the weight loss for an additional 18 months. Rebound weight gain was defined as significant weight loss at 6 months but subsequent regain of body weight during the next 18 months. The results showed that 37 subjects maintained weight loss during 24 months, whereas 36 subjects had rebound weight gain. The BMI at entry and calorie intake and physical activity at each period were similar between the two groups. Subjects who maintained weight loss had at entry a significantly lower fat mass and plasma NE levels compared to those with rebound weight gain. Body fat mass, NE, and leptin levels at entry predicted the degree of change in body weight during the 24-month study period. Subjects with rebound weight gain had a significantly higher frequency of the Gly16 allele for the beta2-adrenoceptor polymorphism compared to subjects who had a 24-month maintenance of weight loss. Subjects carrying the Gly16 allele also had significantly higher plasma NE, leptin, and body fat mass levels and a greater waist-to-hip ratio both at entry and throughout the study. A high initial degree of body fat mass and high plasma NE levels as determined by the Gly16 allele for the beta2-adrenoceptor polymorphisms predict those individuals who will have rebound weight gain after their initial successful weight loss.

Leptin Response and Body Weight Regulation in Humans.

The recent discovery of the positional cloning of the mouse obese (ob) gene has resulted in renewed attention to the scientific study of obesity and body weight regulation. It was further discovered that the ob gene encodes for a circulating hormone, ob protein or leptin. secreted by adipose tissue. In the ob/ob mouse model which becomes very obese, there is a complete leptin deficiency. As such, if leptin is administered to these animals, food intake and body weight decrease significantly. The db/db mouse also becomes obese, but it has high levels of circulating leptin. Thus it is believed that this animal model cannot respond to leptin because of an altered leptin receptor. Because humans appear to have serum leptin levels in proportion to the level of body fat mass it is speculated that leptin resistance may also be involved, at least in part, in the development of human obesity. However, it is also proposed that for normal' body weight regulation, leptin may act like a lipostat in response to changes in energy balance and fat stores and that exogenous leptin could possibly reset the lipostat. Serum leptin levels were measured in three groups of women: those who had lost ≥20% of their body weight and maintained the weight loss: those who lost ≥20% of their body weight and regained it; and weight stable controls who had never dieted. The maintainers and controls had similar leptin levels at 10.2 ± 7.0 and 7.5 ± 3.8 ng/ml respectively. Those who had regained the weight had higher leptin levels than the other two groups at 20.8 ± 8.4 ng/ ml (p 100% predicted) RMR. No relationship between leptin and RMR was observed. There appear to be many unanswered questions about the mechanisms of action of leptin in humans.