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

Insulin-like growth factor II (IGF-II) is a polypeptide that plays a key role in mammalian growth, influencing fetal cell division, differentiation, and possibly metabolic regulation. In adult humans, polymorphisms of the IGF2 gene have been associated with predisposition to obesity. In the present study, we tested the association between IGF2/ApaI genotype and Body Mass Index (BMI) in 294 healthy volunteers (95 men and 199 women; 18-30y) and correlated the results with their birth weights (BW) in order to investigate the relationship between this polymorphic site, fetal life and adult BMI. Blood samples were obtained for DNA extraction, PCR and genotyping. The statistical analyses were performed by the Chi-square, Kolmogorov-Smirnov normality, and Tukey post hoc tests. Although the IGF2 genotype was not significantly associated with BMI and/or BW, we observed a statistically significant correlation of 0.33 (p < 0.023) between BW and BMI in GG subjects whose BW was higher than 3.5 kg (n = 47). We hypothesize that high BWs associated with homozygosis for the G allele of IGF2/ApaI is not a null factor and might be associated with predisposition to high BMI in young adults.
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PMID:Association between birth weight, body mass index and IGF2/ApaI polymorphism. 1610 92

The aim of this study was to examine the effect of aerobic exercise training on insulin sensitivity in overweight and obese girls. Nineteen overweight and obese girls (mean +/- SD: age, 13.1+/-1.8 years; body mass index, 26.8+/-3.9 kg/m(2)) volunteered for this study. Body composition (dual-energy x-ray absorptiometry), insulin sensitivity (oral glucose tolerance test and homeostasis model assessment estimate of insulin resistance; n=15), adiponectin, C-reactive protein (CRP), interleukin (IL) 6, insulin-like growth factor-1, soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 serum levels, and blood lipids and lipoproteins were assessed before and after 12 weeks of aerobic training. Cardiorespiratory fitness increased by 18.8% (P<.05) as a result of training. The area under the insulin concentration curve (insulin area under the curve) decreased by 23.3% (12781.7+/-7454.2 vs 9799.0+/-4918.6 microU.min/mL before and after intervention, respectively; P=.03). Insulin sensitivity was improved without changes in body weight (pre-intervention, 67.9+/-14.5 kg; post-intervention, 68.3+/-14.0 kg) or percent body fat (pre-intervention, 41.4% +/- 4.8%; post-intervention, 40.7%+/-5.2%). The lower limb fat-free mass increased by 6.2% (P<.01) as a result of training, and changes in lower limb fat-free mass were correlated with changes in the insulin area under the curve (r= -.68; P< .01). Serum adiponectin, IL-6, and CRP concentrations did not change (pre-intervention vs post-intervention: adiponectin, 9.57+/-3.01 vs 9.08+/-2.32 microg/mL; IL-6, 1.67+/-1.29 vs 1.65+/-1.25 pg/mL, CRP, 3.21+/-2.48 vs 2.73+/-1.88 mg/L) whereas insulin-like growth factor-1 was lower after training (pre-intervention, 453.8 +/- 159.3 ng/mL; post-intervention, 403.2+/- 155.1 ng/mL; P<.05). In conclusion, 12 weeks of aerobic training improved insulin sensitivity in overweight and obese girls without change in body weight, percent body fat, and circulating concentrations of adiponectin, IL-6, CRP, and other inflammatory markers. These findings suggest that increased physical activity may ameliorate the metabolic abnormalities associated with obesity in children with a mechanism other than the parameters cited earlier.
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PMID:Aerobic exercise training improves insulin sensitivity without changes in body weight, body fat, adiponectin, and inflammatory markers in overweight and obese girls. 1625 36

Fetal overgrowth and higher adiposity are hallmarks of pregnancy with maternal obesity and poor glucose tolerance, two conditions associated with decreased maternal insulin sensitivity. In non-pregnant individuals, adipokines, vasoactive peptides, and components of the immune system crosstalk with metabolic factors to generate signals triggering obesity and impaired insulin action. We have investigated circulating maternal and fetal cytokines and growth-factors as potential biochemical markers of fetal adiposity. Mothers and neonates were classified into three tertiles (T1-T3) using total neonatal fat mass as the outcome with 309 +/- 25 g in T1, 478 +/- 40 g in T2, and 529 +/- 39 g in T3. Umbilical cord endothelin-1 (ET-1), C-peptide, and leptin were higher in T3 and T2 versus T1. Only cord leptin was strongly associated with fetal fat mass (P < .01), whereas neonatal lean body mass was negatively correlated with maternal insulin-like growth factor binding protein-I (IGFBP-I) (r = -0.53, P < .04). This study shows an association between increased fetal adiposity and maternal systemic interleukin-6 (IL-6). No such correlation was found with factors circulating in cord blood, suggesting that the stimuli favoring fetal fat accretion derive from maternal or placental sources rather than from the fetus.
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PMID:Maternal interleukin-6: marker of fetal growth and adiposity. 1637 13

Most of the basic components of the metabolic syndrome, namely type 2 diabetes mellitus, hypertension, obesity, or low high-density lipoprotein cholesterol levels, apart from being major risk factors for cardiovascular disease have been also associated with an increased risk of chronic kidney disease. However, several epidemiologic studies conducted over the past years suggest that the central component of the syndrome, insulin resistance, as well as compensatory hyperinsulinemia are independently associated with an increased prevalence of chronic kidney disease. In addition, background studies support the existence of several pathways linking insulin resistance and hyperinsulinemia with kidney damage. Insulin per se promotes the proliferation of renal cells and stimulates the production of other important growth factors such as insulin-like growth factor-1 and transforming growth factor beta. Insulin also upregulates the expression of angiotensin II type 1 receptor in mesangial cells, thus enhancing the deleterious effects of angiotensin II in the kidney, and stimulates production and renal action of endothelin-1. Moreover, insulin resistance and hyperinsulinemia are associated with decreased endothelial production of nitric oxide and increased oxidative stress which have been also implicated in the progression of diabetic nephropathy. This review analyzes the above and other potential mechanisms, through which insulin resistance and hyperinsulinemia can contribute to renal injury.
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PMID:Insulin resistance, hyperinsulinemia, and renal injury: mechanisms and implications. 1673 48

Growth and nutrition during infancy are being viewed with renewed interest because of the possibility that they may be linked to cardiovascular and metabolic health in later life. Of particular interest are differences between breast- and formula-fed infants with regard to nutrient intake and growth because breastfeeding has been shown to be associated with a reduced risk of obesity in later life. During the first 6-8 weeks of life there is little difference in growth (gain in weight and length) between breast- and formula-fed infants. However, from about 2 months of age to the end of the first year of life formula-fed infants gain weight and length more rapidly than breast-fed infants. There are no consistent differences in adiposity during the first 4-5 months of life, but during the later part of the first year of life the preponderance of the evidence suggests that breast-fed infants are leaner than formula-fed infants. Formula-fed infants at 4-5 months of age show higher plasma levels of insulin-like growth factor-1 (IGF-1), insulin and certain amino acids than breast-fed infants. Whereas the protein intake of breast-fed infants decreases with age and closely matches the requirements for protein during the early months of life, the protein intake of formula-fed infants exceeds requirements after the first 1-2 months of life. The data are consistent with the hypothesis that differences in protein intake are mainly responsible for differences in growth between breast- and formula-fed infants. Differences in energy intake probably are responsible for differences in adiposity observed in older infants.
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PMID:Growth of breast-fed and formula-fed infants. 1690 25

Among other nutrients of breast milk, the amino acid pattern is considered normative throughout infancy. Exclusive breastfeeding by a healthy mother should be the standard from birth to 6 months. During the breastfeeding period the protein intake is low in the human being compared too many other animals. The protein content in breast milk is about 1 g/100 ml and the daily protein intake approximately 1 g/kg/day. When other foods are introduced during the weaning period the protein intake increases remarkably to 3-4 g/kg/day in spite of the fact that the protein requirement is decreasing. The long-term consequences of this phenomenon are obscure. A high protein intake has endocrine effects, such as the high levels of insulin and insulin-like growth factor-1. Furthermore, the metabolic effects with high levels of urea in serum and urine, and the high levels of many amino acids may exceed the capacity of the hepatic and renal systems to metabolize and excrete the excess of nitrogen. This may lead to acidosis and hypernatremic dehydration during periods of fever and diarrhea. Whether the risk of obesity later in life is decreased because of a low intake of protein during the breastfeeding period is still obscure.
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PMID:Effects of high protein intakes. 1690 30

Obesity is associated with multiple endocrine alterations and changes in the concentration of circulating hormones. However, few studies have explored such alterations in dogs with naturally acquired excess weight. In the present study, we investigated the effect of naturally acquired obesity on cortisol, insulin-like growth factor (IGF)-1 and prolactin secretion in dogs. Thirty-one overweight dogs were enrolled in the trial. Blood samples were collected before and after adrenocorticotrophic hormone (ACTH) injection. Free thyroxine (fT4), cortisol, thyroid-stimulating hormone (TSH), IGF-1, prolactin and fructosamine were assayed. Body weight excess increased significantly with age and neutered dogs were more obese than entire ones. The ACTH stimulation test was within the normal range for 26 of 31 dogs. Prolactinaemia was increased in seven dogs and IGF-1 in six dogs. Twenty dogs had a fructosamine concentration >340 microm. Interestingly, 18 of 31 dogs showed disturbances of thyroid function based on high TSH and/or low fT4 baseline concentration, with 11 dogs showing both. According to these parameters only six of 31 dogs were free of hormonal disturbances. These results revealed the high incidence of such disturbances, especially thyroid dysfunction, in obese, but otherwise apparently healthy dogs. They demonstrate the importance of examining endocrine function during the initial evaluation of obese dogs to avoid failure of any nutritional treatment.
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PMID:Hormonal disturbances associated with obesity in dogs. 1695 91

Affecting over 30% of the population, obesity is an epidemic in the United States and is associated with multiple chronic medical problems. Obesity is also associated with numerous hormonal changes, many of which have been implicated in prostate cancer development and progression. Although, on the whole, controversy exists over whether obesity increases the risk of prostate cancer, data strongly suggest that obesity is a significant risk factor for prostate cancer death. In this review, we discuss the epidemiologic data surrounding obesity and prostate cancer. We also discuss some of the sequelae of obesity and their relationships with prostate cancer, including alterations in insulin, the insulin-like growth factor axis, and leptin levels; insulin resistance; and diabetes. Although a complete overview of all the various dietary and lifestyle factors that are associated with obesity and prostate cancer risk is beyond the scope of this review, we discuss data concerning the relationship between a high-fat diet and prostate cancer.
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PMID:Examining the relationship between obesity and prostate cancer. 1698 80

The insulin/insulin-like growth factor signalling (IIS) cascade performs a broad range of evolutionarily conserved functions, including the regulation of growth, developmental timing and lifespan, and the control of sugar, protein and lipid metabolism. Recently, these functions have been genetically dissected in the fruit fly Drosophila melanogaster, revealing a crucial role for cell-surface activation of the downstream effector kinase Akt in many of these processes. However, the mechanisms regulating lipid metabolism and the storage of lipid during development are less well characterized. Here, we use the nutrient-storing nurse cells of the fly ovary to study the cellular effects of intracellular IIS components on lipid accumulation. These cells normally store lipid in a perinuclear pool of small neutral triglyceride-containing droplets. We find that loss of the IIS signalling antagonist PTEN, which stimulates cell growth in most developing tissues, produces a very different phenotype in nurse cells, inducing formation of highly enlarged lipid droplets. Furthermore, we show that the accumulation of activated Akt in the cytoplasm is responsible for this phenotype and leads to a much higher expression of LSD2, the fly homologue of the vertebrate lipid-storage protein perilipin. Our work therefore reveals a signalling mechanism by which the effect of insulin on lipid metabolism could be regulated independently of some of its other functions during development and adulthood. We speculate that this mechanism could be important in explaining the well-established link between obesity and insulin resistance that is observed in Type 2 diabetes.
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PMID:Cytoplasmic activated protein kinase Akt regulates lipid-droplet accumulation in Drosophila nurse cells. 1707 71

Resveratrol (3,5,4'-trihydroxystilbene) extends the lifespan of diverse species including Saccharomyces cerevisiae, Caenorhabditis elegans and Drosophila melanogaster. In these organisms, lifespan extension is dependent on Sir2, a conserved deacetylase proposed to underlie the beneficial effects of caloric restriction. Here we show that resveratrol shifts the physiology of middle-aged mice on a high-calorie diet towards that of mice on a standard diet and significantly increases their survival. Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) activity, increased mitochondrial number, and improved motor function. Parametric analysis of gene set enrichment revealed that resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways. These data show that improving general health in mammals using small molecules is an attainable goal, and point to new approaches for treating obesity-related disorders and diseases of ageing.
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PMID:Resveratrol improves health and survival of mice on a high-calorie diet. 1708 97


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