Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Catch-up growth in previously growth-restricted children is a suggested risk factor for chronic disease risk. We use data from 2026 Filipino adolescents to identify periods of growth that matter more for risk of high blood pressure (BP). Subjects were drawn from the Cebu Longitudinal Health and Nutrition Survey, which enrolled pregnant women and followed up their offspring through age 14 to 16 years. High BP was defined as the top 10% of residuals from gender-specific regressions of systolic and diastolic BP on age and height. After controlling for birth length, current body mass index, age, and height, the odds of high BP in males were significantly decreased with each kilogram increase in birth weight. The highest odds of elevated BP occurred among males who were relatively thin at birth but relatively heavy as adolescents. Larger weight increments from birth to 2 years decreased the odds of high BP in boys, whereas larger increments from 8 to 11 and 11 to 16 years increased the odds of high BP. Thinness at birth significantly interacted with growth rate after age 8, such that a high rate of weight gain increased risk only among boys who were in the lower two thirds of the body mass index distribution at birth. Results in girls indicated small or no effects of early growth. The synergistic effect on adolescent BP of rapid weight gain from late childhood into adolescence with thinness at birth is further evidence of fetal programming of BP in males and suggests long-term health risks associated with rapid growth, even in the absence of obesity.
 ...
PMID:Rapid child growth raises blood pressure in adolescent boys who were thin at birth. 1262 42

Catch-up growth is a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases. We show here that after growth arrest by semistarvation, rats refed the same amount of a low-fat diet as controls show 1) lower energy expenditure due to diminished thermogenesis that favors accelerated fat deposition or catch-up fat and 2) normal glucose tolerance but higher plasma insulin after a glucose load at a time point when their body fat and plasma free fatty acids (FFAs) have not exceeded those of controls. Isocaloric refeeding on a high-fat diet resulted in even lower energy expenditure and thermogenesis and increased fat deposition and led to even higher plasma insulin and elevated plasma glucose after a glucose load. Stepwise regression analysis showed that plasma insulin and insulin-to-glucose ratio after the glucose load are predicted by variations in efficiency of energy use (i.e., in thermogenesis) rather than by the absolute amount of body fat or plasma FFAs. These studies suggest that suppression of thermogenesis per se may have a primary role in the development of hyperinsulinemia and insulin resistance during catch-up growth and underscore a role for suppressed thermogenesis directed specifically at catch-up fat in the link between catch-up growth and chronic metabolic diseases.
 ...
PMID:A role for suppressed thermogenesis favoring catch-up fat in the pathophysiology of catch-up growth. 1271 37

Catch-up growth, a risk factor for later obesity, type 2 diabetes, and cardiovascular diseases, is characterized by hyperinsulinemia and an accelerated rate for recovering fat mass, i.e., catch-up fat. To identify potential mechanisms in the link between hyperinsulinemia and catch-up fat during catch-up growth, we studied the in vivo action of insulin on glucose utilization in skeletal muscle and adipose tissue in a previously described rat model of weight recovery exhibiting catch-up fat caused by suppressed thermogenesis per se. To do this, we used euglycemic-hyperinsulinemic clamps associated with the labeled 2-deoxy-glucose technique. After 1 week of isocaloric refeeding, when body fat, circulating free fatty acids, or intramyocellular lipids in refed animals had not yet exceeded those of controls, insulin-stimulated glucose utilization in refed animals was lower in skeletal muscles (by 20-43%) but higher in white adipose tissues (by two- to threefold). Furthermore, fatty acid synthase activity was higher in adipose tissues from refed animals than from fed controls. These results suggest that suppressed thermogenesis for the purpose of sparing glucose for catch-up fat, via the coordinated induction of skeletal muscle insulin resistance and adipose tissue insulin hyperresponsiveness, might be a central event in the link between catch-up growth, hyperinsulinemia and risks for later metabolic syndrome.
 ...
PMID:Redistribution of glucose from skeletal muscle to adipose tissue during catch-up fat: a link between catch-up growth and later metabolic syndrome. 1573 52

Most children who are short or light at birth due to intrauterine growth restriction (IUGR) exhibit accelerated growth in infancy, termed "catch-up" growth, which together with IUGR, predicts increased risk of type 2 diabetes and obesity later in life. Placental restriction (PR) in sheep reduces size at birth, and also causes catch-up growth and increased adiposity at 6 wk of age. The physiological mechanisms responsible for catch-up growth after IUGR and its links to these adverse sequelae are unknown. Because insulin is a major anabolic hormone of infancy and its actions are commonly perturbed in these related disorders, we hypothesized that restriction of fetal growth would alter insulin secretion and sensitivity in the juvenile sheep at 1 month, which would be related to their altered growth and adiposity. We show that PR impairs glucose-stimulated insulin production, but not fasting insulin abundance or production in the young sheep. However, PR increases insulin sensitivity of circulating free fatty acids (FFAs), and insulin disposition indices for glucose and FFAs. Catch-up growth is predicted by the insulin disposition indices for amino acids and FFAs, and adiposity by that for FFAs. This suggests that catch-up growth and early-onset visceral obesity after IUGR may have a common underlying cause, that of increased insulin action due primarily to enhanced insulin sensitivity, which could account in part for their links to adverse metabolic and related outcomes in later life.
 ...
PMID:Placental restriction of fetal growth increases insulin action, growth, and adiposity in the young lamb. 1711 Apr 32

This paper gives an overview of studies with the main purpose to intervene against obesity in children at the school arena. Through databases and Cochrane reviews, 14 studies fulfilled the criteria for inclusion. Most of the studies are American and none were performed in Scandinavia. The European studies were performed in Germany and in the United Kingdom. The studies, which had a significant effect on overweight were 'Dance for Health', 'Planet Health', 'San Jose Study', 'Kiel Obesity Prevention Study', 'Healthy Schools' programme, 'El Paso Catch', and 'Medical College of Georgia FitKid Project'. The studies differ greatly in regards to age group, type of and length of intervention and type and amount of actions. Furthermore, the measures used to evaluate the effect differed. It seems to be important to use several measures of obesity in order to accurately detect a possible effect. In conclusion, half of the studies were successful and had an effect on either overweight or obesity. Much more research is needed in order to effectively prevent paediatric obesity.
 ...
PMID:Prevention of overweight in the school arena. 1731 9

Catch-up growth early in life (after fetal, neonatal or infantile growth retardation) is a major risk factor for later obesity, type-2 diabetes and cardiovascular diseases. These risks are generally interpreted alongside teleological arguments that environmental exposures which hinder growth early in life lead to programming of 'thrifty mechanisms' that are adaptive during the period of limited nutrient supply (or growth constraint), but which increase risks for diseases during improved nutrition and catch-up growth later in life. This paper addresses this notion of 'thrifty mechanisms' in the light of evidence that catch-up growth is characterized by a disproportionately higher rate of fat gain relative to lean tissue gain, and that such preferential catch-up fat is in part driven by energy conservation mechanisms operating via suppressed thermogenesis. It provides a molecular-physiological framework which integrates emerging insights into mechanisms by which this thrifty 'catch-up fat' phenotype cross-links with insulin and leptin resistance.
 ...
PMID:Thrifty energy metabolism in catch-up growth trajectories to insulin and leptin resistance. 1827 86

Growth faltering occurs frequently in infancy in the 22q11 Deletion syndrome (22q11 DS). The subsequent course of growth in childhood and outcome for final adult height lacks consensus. We analyzed 5,149 growth data points from 812 Caucasian subjects with 22q11 DS, from neonates to 37 years old. Charts were constructed for height, weight, body mass index, and head circumference (OFC) using the LMS Chart Maker program. These charts were compared with the WHO birth to 4 years growth standard and US CDC 2000 growth reference between 5 and 20 years. Starting from the 50th centile at birth, by 6-9 months of age boys mean height and weight had fallen to the 9th centile, as did girls height but their weight fell less markedly, to the 25th centile. Feeding difficulties were non-contributory. In children under 2 years old with congenital heart disease (CHD) mean weight was -0.5 SD lighter than no CHD. Catch up growth occurred, more rapid in weight than height in boys. Up to 10 years old both sexes tracked between the 9th and 25th centiles. In adolescence, the trend was to overweight rather than obesity. At 19 years mean height was -0.72 SD for boys, -0.89 SD girls. OFC was significantly smaller than the WHO standard in infancy, between the 9th and 25th centile, rising to the 25th centile by 5 years old. Thereafter the mean was close to the 9th centile of the OFC UK growth reference, more prolonged and marked than in previous studies.
 ...
PMID:Syndrome-specific growth charts for 22q11.2 deletion syndrome in Caucasian children. 2271 Dec 68

Cigarette smoking is an addictive behavior, and is the primary cause of cardiovascular and pulmonary disease, and cancer (among other diseases). Cigarette smoke contains thousands of components that may affect caloric intake and energy expenditure, although nicotine is the major addictive substance present, and has the best described actions. Nicotine exposure from cigarette smoke can change brain feeding regulation to reduce appetite via both energy homeostatic and reward mechanisms, causing a negative energy state which is characterized by reduced energy intake and increased energy expenditure that are linked to low body weight. These findings have led to the public perception that smoking is associated with weight loss. However, its effects at reducing abdominal fat mass (a predisposing factor for glucose intolerance and insulin resistance) are marginal, and its promotion of lean body mass loss in animal studies suggests a limited potential for treatment in obesity. Smoking during pregnancy puts pressure on the mother's metabolic system and is a significant contributor to adverse pregnancy outcomes. Smoking is a predictor of future risk for respiratory dysfunction, social behavioral problems, cardiovascular disease, obesity, and type-2 diabetes. Catch-up growth is normally observed in children exposed to intrauterine smoke, which has been linked to subsequent childhood obesity. Nicotine can have a profound impact on the developing fetal brain, via its ability to rapidly and fully pass the placenta. In animal studies this has been linked with abnormal hypothalamic gene expression of appetite regulators such as downregulation of NPY and POMC in the arcuate nucleus of the hypothalamus. Maternal smoking or nicotine replacement leads to unhealthy eating habits (such as junk food addiction) and other behavioral disorders in the offspring.
 ...
PMID:Cigarette smoking and brain regulation of energy homeostasis. 2284 2

Childhood overweight and obesity disproportionately affect low-income communities. Most school-based health promotion efforts occur during the school day and are limited in scope. This study evaluated the effectiveness of an after-school program among 3rd-5th graders (n=121; 73% 8 to 9 years old; 57% female; 60% Asian) at eight study sites (four intervention, four comparison). After-school staff were trained on implementing the Catch Kids Club Curriculum on nutrition and physical activity. Data were collected on students' nutrition and physical activity knowledge and behavior, and their height and weight measurements. Using Stata 10.1/SE, cross-lagged regression models assessed changes over time. Results showed a reduction in overweight and obesity (defined as body mass index >85th percentile for age and sex) among children in the intervention group, but mixed results regarding diet and physical activity knowledge and behavior. Enhancing after-school physical activity opportunities through evidence-based programs can potentially improve overweight and obesity among low-income children.
 ...
PMID:Improving overweight among at-risk minority youth: results of a pilot intervention in after-school programs. 2372 61

Increased focus on the potential negative side effects of steroid usage in pediatric transplantation has led to steroid minimization or steroid-free transplantation. In this study, we report results after complete steroid avoidance in renal transplantation in the period 1994-2009. We evaluate the effects of complete steroid avoidance on allograft function, BMI, and linear growth. The majority of transplanted children were induced with antithymocyte globulin and immunosuppressed with a calcineurin inhibitor and mycophenolate mofetil. Steroids were given only when rejection occurred or due to comorbidities. Anthropometric data were collected from 65 transplantations in 60 children. Patient survival was 93%; graft survival was 81% after five yr (N = 42) and 63% after 10 yr (N = 16). Acute rejection within the first year of transplantation was 9%. The distribution of the children's BMI before transplantation was normal; the mean BMI-SDS was 0.21 before transplantation, and this value remained stable during the next five yr. Post-transplantation the children demonstrated significant improved growth as the mean height-SDS increased significantly from -1.7 to -1.1. Catch-up growth was most pronounced in the youngest (< six yr). Steroid-free immunosuppression in pediatric renal transplantation is safe and protects against steroid-induced obesity and short stature.
 ...
PMID:Long-term experience of steroid-free pediatric renal transplantation: effects on graft function, body mass index, and longitudinal growth. 2438 46


1 2 Next >>