- C.P.G.M. Groot de (1)
- B. Hoebee (1)
- A. Jung (1)
- B.H. Knopfli (1)
- S.B. Murer (1)
- C.T.M. Rossum van (1)
- W.H.M. Saris (1)
- J.C. Seidell (1)
- J. Wildhaber (1)
- J. Wildhaber-Brooks (1)
- M.B. Zimmermann (1)
During Rapid Weight Loss in Obese Children, Reductions in TSH Predict Improvements in Insulin Sensitivity Independent of Changes in Body Weight or Fat
Aeberli, I. ; Jung, A. ; Murer, S.B. ; Wildhaber, J. ; Wildhaber-Brooks, J. ; Knopfli, B.H. ; Zimmermann, M.B. - \ 2010
Journal of Clinical Endocrinology and Metabolism 95 (2010)12. - ISSN 0021-972X - p. 5412 - 5418.
coronary-heart-disease - subclinical hypothyroidism - thyroid-function - reference range - morbid-obesity - in-vivo - leptin - risk - adolescents - population
Background: Although serum TSH is often elevated in obesity and may be linked to disorders of lipid and glucose metabolism, the clinical relevance of these relationships remains unclear. Subjects: Subjects were obese children and adolescents (n = 206; mean age 14 yr) undergoing rapid weight and fat loss in a standardized, multidisciplinary, 2-month, in-patient weight loss program. Design: This was a prospective study that determined thyroid function, glucose and lipid parameters, leptin, anthropometric measures, and body composition measured by dual-energy x-ray absorption at baseline and at the end of the intervention. Results: At baseline, 52% of children had TSH concentrations in the high normal range (> 2.5 mU/liter), but TSH was not correlated with body weight, body mass index SD scores, lean body mass, or body fat percentage. At baseline, independent of adiposity, TSH significantly correlated with total cholesterol (P = 0.008), low-density lipoprotein cholesterol (P = 0.013), fasting insulin (P = 0.010), homeostatic model assessment (HOMA) (P = 0.004), and leptin (P = 0.006). During the intervention, mean body fat, TSH, HOMA, and fasting insulin decreased by 21, 11, 53, and 54%, respectively. Change (Delta) in TSH did not correlate with Delta body weight or Delta body composition, but Delta TSH significantly correlated with, Delta fasting insulin and Delta HOMA, independent of Delta body weight or Delta body composition (P <0.05). Conclusion: TSH concentrations are elevated in obese children but are not correlated with the amount of excess body weight or fat. During weight loss, independent of changes in body weight or composition, decreases in elevated serum TSH predict decreases in fasting insulin and HOMA. These findings suggest interventions that target high TSH concentrations during weight loss in obese subjects may improve insulin sensitivity. (J Clin Endocrinol Metab 95: 5412-5418, 2010)
Genetic factors as predictors of weight gain in young adult Dutch men and women
Rossum, C.T.M. van; Hoebee, B. ; Seidell, J.C. ; Bouchard, C. ; Baak, M.A. van; Groot, C.P.G.M. de; Chagnon, M. ; Graaf, C. de; Saris, W.H.M. - \ 2002
International Journal of Obesity 26 (2002)4. - ISSN 0307-0565 - p. 517 - 528.
body-mass index - uncoupling protein-2 gene - leptin receptor gene - juvenile-onset obesity - gamma-gene - pro12ala variant - morbid-obesity - beta(2)-adrenoceptor gene - adrenoceptor genes - insulin-resistance
OBJECTIVE: To investigate the association between DNA polymorphisms in several candidate genes for obesity and weight gain. Polymorphisms in these genes may contribute to weight gain through effects on energy intake, energy expenditure or adipogenesis. DESIGN AND METHODS: From two large cohorts in The Netherlands (total 17,500 adult men and women), we compared 286 subjects aged 20-40 y who gained an average of 12.8 kg (range 5.5-47 kg) during a mean follow-up of 6.8 y with 296 subjects who remained relatively constant over the same period with respect to occurrence of several polymorphisms in candidate genes of obesity and some lifestyle factors. Subjects who were dieting, were high alcohol consumers, were pregnant, changed their smoking status recently, or those who suffered from serious illnesses were excluded. Polymorphisms were determined in the LEPR-gene (LEPR Lys109Arg, LEPR Gln223Arg, LEPR Lys656Asn), in the UCP1 gene (A-G mutation at position-3826 5' region), in the UCP2 gene (Ala55Val, 45 bp Ins/Del), in the PPARG2 gene (Pro12Ala) and in the ADRB2 gene (Gly16Arg and Gln27Glu). RESULTS: With the exception of the Gly16Arg polymorphism in the ADRB2 gene in men (P = 0.04) and women (P = 0.05), and the Lys109Arg polymorphism in the LEPR gene in women, no statistically significant differences in the genotype and allele frequencies were observed between weight gainers and non-weight gainers. Weight gainers differed in some aspects of dietary habits and physical activity patterns: weight gainers consumed relatively more savory snacks and were less active during leisure time compared with non-weight gainers. CONCLUSION: Only variations in the ADRB2 gene and LEPR gene, may contribute to susceptibility to weight gain. None of the other studied genetic markers were clearly associated with weight gain. Further research is necessary to establish the role of lifestyle factors, or interactions between genes or between genes and lifestyle factors on weight gain with age.