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• W2043910227 abstract "See related articles, p 472 and p 477. The population geneticist J. V. Neel proposed the “thrifty genotype” hypothesis in 1962 to explain the emergence of type 2 diabetes in populations shifting from vigorous activity and subsistence nutrition to indolence, abundance, and consequent obesity.1Neel JV Diabetes mellitus: A “thrifty” genotype rendered detrimental by “progress”?.Am J Hum Genet. 1962; 14: 353-362PubMed Google Scholar He suggested that metabolic characteristics permitting survival in a feast-and-famine existence, such as an enhanced ability to store energy as fat, would become detrimental with abundant food. Considerable evidence has accumulated for possible mechanisms of expression of this genotype. For example, the degree of insulin resistance (IR) and the concomitant risk of type 2 diabetes correlates with visceral obesity, ie, the fat depot that is most mobile and thus most responsive to feasting and available for energy during fasting.2Caprio S Tamborlane WV Metabolic impact of obesity in childhood.Endocrinol Metab Clin North Am. 1999; 28: 731-747Abstract Full Text Full Text PDF PubMed Scopus (78) Google Scholar Another example of possible expression of the thrifty genotype is that African American youngsters, in addition to having greater baseline and glucose-stimulated insulin levels, have lower rates of lipolysis and both lower resting energy expenditure and maximal oxygen consumption with exercise (are more thrifty) than age, sex, and body mass index (BMI)-matched white children.3Svec F Nastasi K Hilton C Bao W Srinivasan SR Berenson GS Black-white contrasts in insulin levels during pubertal development. The Bogalusa Heart Study.Diabetes. 1992; 41: 313-317Crossref PubMed Scopus (153) Google Scholar, 4Kaplan AS Zemel BS Stallings VA Differences in resting energy expenditure in prepubertal black children and white children.J Pediatr. 1996; 129: 643-647Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar, 5Morrison JA Alfaro MP Khoury P Thornton BB Daniels SR Determinants of resting energy expenditure in young black girls and young white girls.J Pediatr. 1996; 129: 637-642Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar, 6Arslanian S Insulin secretion and sensitivity in healthy African-American vs American-white children.Clin Pediatr. 1998; 37: 81-88Crossref PubMed Scopus (57) Google Scholar, 7Uwaifo GI Nguyen TT Keil MF Russell DL Nicholson JC Bonat SH et al.Differences in insulin secretion and sensitivity of Caucasian and African-American prepubertal children.J Pediatr. 2002; 140: 673-680Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 8Li C Johnson MS Goran MI Effects of low birth weight on insulin resistance syndrome in Caucasian and African American children.Diabetes Care. 2001; 24: 2035-2042Crossref PubMed Scopus (108) Google ScholarAfrican American prepubertal and pubertal children also have lower C-peptide/insulin molar ratios than white children, suggesting lower hepatic clearance of insulin as an inherent contributor to hyperinsulinism.7Uwaifo GI Nguyen TT Keil MF Russell DL Nicholson JC Bonat SH et al.Differences in insulin secretion and sensitivity of Caucasian and African-American prepubertal children.J Pediatr. 2002; 140: 673-680Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar, 9Jiang X Srinivasan SR Radhakrishnamurthy B Dalferes ER Berenson GS Racial (black-white) differences in insulin secretion and clearance in adolescents: The Bogalusa Heart Study.Pediatrics. 1996; 97: 357-360PubMed Google Scholar Elevated circulating insulin concentrations as the result of relative insulin insensitivity might also delay the onset of satiety, permitting greater energy storage. Nearly 3 decades after Neel's proposal, a remarkable series of epidemiologic studies of older adults in the United Kingdom, for whom birth records were available, demonstrated that small size at birth, not related to prematurity, was associated with increased risk for visceral obesity, hypertension, type 2 diabetes, and coronary heart disease, all components of what has come to be recognized as the IR syndrome.10Barker DJ Winter PD Osmond C Margetts B Simmonds SJ Weight in infancy and death from ischaemic heart disease.Lancet. 1989; ii: 577-580Abstract Scopus (2554) Google Scholar, 11Barker DJ Bull AR Osmond C Simonds SJ Fetal and placental size and risk of hypertension in adult life.BMJ. 1990; 301: 259-262Crossref PubMed Scopus (1406) Google Scholar, 12Hales CN Barker DJ Clark PM Cox LJ Fall C Osmond C et al.Fetal and infant growth and impaired glucose tolerance at age 64.BMJ. 1991; 303: 1019-1022Crossref PubMed Scopus (2205) Google Scholar, 13Hales CN Barker DJ Type 2 (non-insulin-dependent) diabetes mellitus: The thrifty phenotype hypothesis.Diabetologia. 1992; 35: 595-601Crossref PubMed Scopus (2500) Google Scholar, 14Barker DJ Hales CN Fall CH Osmond C Phipps K Clark PM Type 2 (non-insulin-dependent) diabetes mellitus, hypertension and hyperlipidaemia (syndrome X): Relation to reduced fetal growth.Diabetologia. 1993; 36: 62-67Crossref PubMed Scopus (2145) Google Scholar, 15Barker DJ Osmond C Simmonds SJ Wield GA The relation of small head circumference and thinness at birth to death from cardiovascular disease in adult life.BMJ. 1993; 306: 422-426Crossref PubMed Scopus (599) Google Scholar, 16Osmond C Barker DJ Winter PD Fall CH Simmonds SJ Early growth and death from cardiovascular disease in women.BMJ. 1993; 307: 1519-1524Crossref PubMed Scopus (609) Google Scholar, 17Phipps K Barker DJP Fetal growth and impaired glucose tolerance in men and women.Diabetologia. 1993; 36: 225-228Crossref PubMed Scopus (459) Google Scholar, 18Philips DIW Barker DJP Hales CN Hirst S Osmond C Thinness at birth and insulin resistance in adult life.Diabetologia. 1994; 37: 150-154Crossref PubMed Scopus (616) Google Scholar Studies in the United States, Sweden, India, and South Africa have confirmed the findings from the United Kingdom.19Lithell HO McKeigue PM Berglund L Mohsen R Lithell UB Leon DA Relation of size at birth to non-insulin-dependent diabetes and insulin concentrations in men aged 50-60 years.BMJ. 1996; 312: 406-410Crossref PubMed Scopus (637) Google Scholar, 20Curhan GC Willett WC Rimm EB Spiegelman D Ascherio AL Stampfer MJ Birth weight and adult hypertension, diabetes mellitus, and obesity in US men.Circulation. 1996; 94: 3246-3250Crossref PubMed Scopus (781) Google Scholar, 21Fall CH Stein CE Kumaran K Cox V Osmond C Barker DJ et al.Size at birth, maternal weight, and type 2 diabetes in South India.Diabet Med. 1998; 15: 220-227Crossref PubMed Scopus (229) Google Scholar, 22Levitt NS Lambert EV Woods D Hales CN Andrew R Seckl R Impaired glucose tolerance and elevated blood pressure in low birthweight, nonobese, young South African adults: Early programming of cortisol axis.J Clin Endocrinol Metab. 2000; 85: 4611-4618Crossref PubMed Scopus (256) Google Scholar Glucose intolerance was also found in Dutch adults whose mothers starved during the last trimester of pregnancy during the famine of World War II.23Ravelli AC van der Meulen JH Michels RP Michels RP Osmond C Barker DJ et al.Glucose tolerance in adults after prenatal exposure to famine.Lancet. 1998; 351: 173-177Abstract Full Text Full Text PDF PubMed Scopus (1217) Google Scholar The observations of the UK investigators led to the thrifty phenotype hypothesis, that poor nutrition in fetal and early infant life would be detrimental to the development and function of the β cells and insulin-sensitive tissues, primarily muscle, leading to insulin insensitivity and, with the added IR of obesity later in life, type 2 diabetes.16Osmond C Barker DJ Winter PD Fall CH Simmonds SJ Early growth and death from cardiovascular disease in women.BMJ. 1993; 307: 1519-1524Crossref PubMed Scopus (609) Google Scholar Obviously, small size at birth not caused by prematurity could also be genetically determined, and one such mechanism could be through defective insulin action in utero. The rare congenital syndromes of IR are associated with intrauterine growth failure, emphasizing the importance of insulin as a fetal growth factor. The implication of intrauterine growth restriction (IUGR) in chronic diseases of adulthood that are associated with IR led pediatric investigators to explore IR in childhood in relationship to fetal growth. The relevance of this quest was heightened by the epidemic of type 2 diabetes in the pediatric population during the past decade.24Fagot-Campagna A Pettitt DJ Engelgau MM Burrows NR Geiss LS Valdez R et al.Type 2 diabetes among North American children and adolescents: An epidemiological review and a public health perspective.J Pediatr. 2000; 136: 664-672Abstract Full Text PDF PubMed Scopus (934) Google Scholar Current body weights of 5- to 29-year-old Pima Indians (n = 3061) correlated with their birth weights, and 2-hour postglucose ingestion glucose concentrations had a U-shaped relationship with birth weight in subjects older than ten years, regardless of their current body weight.25Dabelea D Pettitt DJ Hanson RL Imperatore G Bennett PH Knowler WC Birthweight, type 2 diabetes, and insulin resistance in Pima Indian children and young adults.Diabetes Care. 1999; 22: 944-950Crossref PubMed Scopus (224) Google Scholar Thus both overweight and underweight at birth are associated with a greater risk for diabetes.26Ong KKL Dunger DB Thrifty genotypes and phenotypes in the pathogenesis of type 2 diabetes mellitus.J Pediatr Endocrinol Metab. 2000; 13: 1419-1424PubMed Google Scholar Short prepubertal children who had IUGR had increased insulin responses and decreased insulin sensitivity compared with age- and sex-matched children with normal birth weights for age.27Hofman PL Cutfield WS Robinson EM Bergman RN Menon RK Sperling MA et al.Insulin resistance in short children with intrauterine growth retardation.J Clin Endocrinol Metab. 1997; 82: 402-406Crossref PubMed Scopus (413) Google Scholar IR variables and plasma total and low-density lipoprotein cholesterol levels strongly related to current body weight in 477 Indian children aged 8 years; lower birth weight, the result of poor nutrition, was associated with elevated systolic blood pressure, elevated fasting plasma insulin, and 32 to 33 split pro-insulin concentrations (an indicator of β cell dysfunction), elevated glucose and insulin concentrations after glucose administration, higher plasma lipids, and higher calculated IR. The highest risks were associated with low birth weight and high fat mass at 8 years of age.28Bavdekar A Yajnik CS Fall CHD Bapat S Pandit AN Deshpande V et al.Insulin resistance syndrome in 8-year old Indian children. Small at birth, big at 8 years, or both?.Diabetes. 1999; 48: 2422-2429Crossref PubMed Scopus (540) Google Scholar Virtually identical findings have been described among 400 Jamaican children aged 7.5 years to 10.5 years.29Bennett F Watson-Brown C Thame M Wilks R Osmond C Hales N et al.Shortness at birth is associated with insulin resistance in prepubertal Jamaican children.Eur J Clin Nutr. 2002; 56: 506-511Crossref PubMed Scopus (15) Google Scholar Young adults who were intrauterine growth restricted were found to have increased body fat compared with BMI-matched controls and to have lower insulin-stimulated glucose uptake, which persisted with correction for total body fat and visceral fat.30Jaquet D Gaboriau A Czernichow P Levy-Marchal C Insulin resistance early in adulthood in subjects with intrauterine growth retardation.J Clin Endocrinol Metab. 2000; 85: 1401-1406Crossref PubMed Scopus (336) Google Scholar It is likely that environmentally caused or genetically determined IUGR would have similar effects on growth and development of pancreatic β cells and insulin sensitive tissues. The expression of the glucose transporter gene (GLUT4) in muscle and fat is impaired in young adults who had IUGR, an effect that could reflect genetic predisposition or be secondary to altered cellular growth and development from nutritional limitation.31Jaquet D Vidal H Hankard R Czernichow P Levy-Marchal C Impaired regulation of glucose transporter 4 gene expression in insulin resistance associated with in utero undernutrition.J Clin Endocrinol Metab. 2001; 86: 3266-3271PubMed Google Scholar A genetic link between the insulin gene, glucose sensing in the pancreas and other tissues, size at birth, and type 2 diabetes later in life has been provided by several studies. Inheritance of a glucokinase mutation by the fetus has been associated with a reduction in birth weight, and could be linked to the risk of type 2 diabetes.32Hattersley AT Beards F Ballantyne E Appleton M Harvey R Ellard S Mutations in the glucokinase gene of the fetus result in reduced birthweight.Nat Genet. 1998; 19: 268-270Crossref PubMed Scopus (481) Google Scholar This mechanism involving a rare defect is unlikely to have widespread applicability. In a cohort study in the Avon district of the United Kingdom, the variable number of tandem repeats (VNTR) locus of the insulin gene (INS) was examined for a polymorphism associated with size at birth in 758 term births. Significant genetic associations were found with length, weight, and head circumference at birth.33Dunger DB Ong KK Huxtable SJ Sherriff A Woods KA Ahmed ML et al.Association of the INS VNTR with size at birth. ALSPAC study team. Avon longitudinal study of pregnancy and childhood.Nat Genet. 1998; 19: 98-100Crossref PubMed Scopus (257) Google Scholar Also described by this group was an association between a variant mitochondrial DNA (ie, transmitted maternally) and thinness at birth and the risk of type 2 diabetes in men from the original UK epidemiologic studies.34Ong KK Ahmed ML Emmett PM Preece MA Dunger DB The insulin gene VNTR, type 2 diabetes and birth weight.Nat Genet. 1999; 21: 262-263Crossref PubMed Scopus (149) Google Scholar This observation of a maternally transmitted trait, together with the realization that the INS VNTR phenotype that is associated with larger fetal size is paternally transmitted, is reminiscent of the “tug-of-war” between the paternally expressed potent fetal growth factor insulin-like growth factor-II, and its maternally expressed receptor, which would constrain fetal growth, protecting the mother.35Moore T Haig D Genomic imprinting in mammalian development: A parental tug-of-war.Trends Genet. 1991; 7: 45-49Abstract Full Text PDF PubMed Scopus (929) Google Scholar Within this complex interplay of known, speculative, and unknown variables affecting intrauterine growth and insulin sensitivity, Leipälä et al36Leipälä JA Raivio KO Sarnesto A Panteleon A Fellman V Intrauterine growth restriction and postnatal steroid effects on insulin sensitivity in preterm neonates.J Pediatr. 2002; 141: 472-476Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar report in this issue of The Journal results of a study to evaluate whether IR is present in the first week of life in small-forgestational age (SGA) infants, and whether the mechanism for hyperglycemia with glucocorticoid therapy in infants is the result of IR. The group that they studied differed from subjects in the epidemiologic and the prospective cohort studies described previously because both SGA and appropriate-for-gestational-age (AGA) infants were sufficiently ill to be in the intensive care unit, and all mothers had received prenatal steroids. Five of the 10 AGA infants and 8 of the 13 SGA infants also received steroids postnatally. An attenuated modified minimal model intravenous glucose tolerance test was used to ascertain insulin sensitivity. Did the investigators answer the questions that they were addressing? Although they did not find a difference in insulin sensitivity between the AGA and SGA infants, real differences may have been masked because both groups were ill and had been exposed to prenatal steroids. The range of responses was wide and the numbers small. There was a significantly reduced insulin sensitivity in the SGA group receiving postnatal dexamethasone compared with SGA infants who did not, a difference that did not occur in the AGA group. This observation would be more impressive if it were controlled; the reasons for dexamethasone use may have been a more influential confound in the outcome than the dexamethasone itself. In addition to providing an opportunity to consider the importance of fetal growth in the development of the IR syndrome, the studies of Leipälä et al36Leipälä JA Raivio KO Sarnesto A Panteleon A Fellman V Intrauterine growth restriction and postnatal steroid effects on insulin sensitivity in preterm neonates.J Pediatr. 2002; 141: 472-476Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar and Tenhola et al,37Tenhola S Martikainen A Rabiala E Parviainen M Halonen P Voutilainen R Increased adrenocortical and adrenomedullary hormonal activity in 12-year-old children born small for gestational age.J Pediatr. 2002; 141: 477-482Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar also in this issue of The Journal, induce reflection on the role of the hypothalamic-pituitary-adrenal axis and adrenal medullary activity in this schema. Increased adrenocortical and adrenomedullary excretion have been noted in SGA infants.38Clark PM Hindmarsh PC Schiell A Law CM Honour J Barker DJP Size at birth and adrenocortical function in childhood.Clin Endocrinol. 1996; 45: 721-726Crossref PubMed Scopus (186) Google Scholar, 39Dalmaz Y Peyrin L Dutruge J Sann L Neonatal pattern of adrenergic metabolites in urine of small for gestational age and preterm infants.J Neural Transm. 1980; 49: 151-165Crossref PubMed Scopus (20) Google Scholar, 40Divers WA Wilkes MM Babaknia A Hill LM Quilligan EJ Yen SS Amniotic fluid catecholamines and metabolites in intrauterine growthretardation.Am J Obstet Gynecol. 1981; 141: 608-610Abstract Full Text PDF PubMed Google Scholar In the 3 UK cohorts studied for the relationship between low birth weight and IR manifestations, low birth weight was also found to be associated with raised plasma cortisol concentrations, which correlated with current blood pressure.41Philips DIW Barker DJP Fall CHD Seckl JR Whorwood CB Wood PJ et al.Elevated plasma cortisol concentrations: A link between low birth weight and the insulin resistance syndrome?.J Clin Endocrinol Metab. 1998; 83: 757-760PubMed Google Scholar, 42Phillips DI Walker BR Reynolds RM Flanagan DE Wood PJ Osmond C et al.Low birth weight predicts elevated plasma cortisol concentrations in adults from 3 populations.Hypertension. 2000; 35: 1301-1306Crossref PubMed Scopus (344) Google Scholar Among 20-year-old historically disadvantaged urbanized South African subjects, those who were underweight for age at birth were smaller, lighter, and had a lower BMI than subjects who had been AGA, but with higher fasting plasma glucose, more frequent glucose intolerance (12% vs 0%), higher blood pressure, and higher morning plasma cortisol levels and response to adrenocorticotropic hormone. It was considered that cortisol axis activation was an early feature linking low birth weight with adult cardiovascular and metabolic disease.22Levitt NS Lambert EV Woods D Hales CN Andrew R Seckl R Impaired glucose tolerance and elevated blood pressure in low birthweight, nonobese, young South African adults: Early programming of cortisol axis.J Clin Endocrinol Metab. 2000; 85: 4611-4618Crossref PubMed Scopus (256) Google Scholar Indeed, studies in rats have suggested that glucocorticoid exposure late in pregnancy predisposes the offspring to glucose intolerance in adulthood.43Nyirenda MJ Lindsay RS Kenyon CJ Burchell A Seckl JR Glucocorticoid exposure in late gestation permanently programs phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring.J Clin Invest. 1998; 101: 2174-2181Crossref PubMed Scopus (506) Google Scholar Especially important is the type of glucocorticoid. The fetus is normally protected from elevated maternal levels of glucocorticoid by fetoplacental 11β hydroxysteroid dehydrogenase type 2, which converts active cortisol to inactive cortisone; dexamethasone is a poor substrate for this enzyme and, therefore, more likely to induce changes that mimic fetal undernutrition, an important consideration for interpreting the study of Leipälä et al.36Leipälä JA Raivio KO Sarnesto A Panteleon A Fellman V Intrauterine growth restriction and postnatal steroid effects on insulin sensitivity in preterm neonates.J Pediatr. 2002; 141: 472-476Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar The elevation of fetal corticotropin and cortisol levels in IUGR,44Goland RS Josak S Warren WB Cornwell IM Stark RI Tropper PJ Elevated levels of umbilical cord plasma corticotropin releasing hormone in growth retarded fetuses.J Clin Endocrinol Metab. 1993; 77: 1174-1179Crossref PubMed Google Scholar together with the evidence for an effect of fetal undernutrition on long-term hypothalamic-pituitary-adrenal and adrenomedullary activation,37Tenhola S Martikainen A Rabiala E Parviainen M Halonen P Voutilainen R Increased adrenocortical and adrenomedullary hormonal activity in 12-year-old children born small for gestational age.J Pediatr. 2002; 141: 477-482Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar provides a credible hypothesis for further exploration linking fetal development and later disease, including hypertension, central adiposity, and impaired glucose tolerance, which are problems consistent with chronic elevated fasting cortisol and epinephrine levels. Appreciation of this possibility adds caution to the perinatal use of steroid therapy, and, as noted by Leipälä et al,36Leipälä JA Raivio KO Sarnesto A Panteleon A Fellman V Intrauterine growth restriction and postnatal steroid effects on insulin sensitivity in preterm neonates.J Pediatr. 2002; 141: 472-476Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar the possible long-term effects of such therapy remain to be defined. It is important that these investigators and others pursue the necessary long-term studies of children who have received perinatal glucocorticoids. Intrauterine growth restriction and postnatal steroid treatment effects on insulin sensitivity in preterm neonatesThe Journal of PediatricsVol. 141Issue 4PreviewObjectives: To study whether intrauterine growth restriction (IUGR) is associated with decreased sensitivity to the main fetal growth factor, insulin, and the effect of glucocorticoid therapy on insulin sensitivity in preterm infants. Study design: Newborn infants with a birth weight (BW) of< 1500 g were classified as appropriate for gestational age ([AGA], BW within ± 1 SD, n = 10), or small for gestational age ([SGA], BW <–2 SD, n = 13); 5 AGA infants and 8 SGA infants received systemic steroids. Full-Text PDF Increased adrenocortical and adrenomedullary hormonal activity in 12-year-old children born small for gestational ageThe Journal of PediatricsVol. 141Issue 4PreviewObjectives: To determine whether adrenal hormonal activity is altered in children born small for gestational age (SGA), and whether concentrations of adrenal hormones relate to those of serum lipids or to anthropometric measures. Study design: We studied 55 SGA children and 55 appropriate for gestational age (AGA) children at the age of 12 years in a case-control setting. The concentrations of fasting serum cortisol, dehydroepiandrosterone sulfate (DHEAS), plasma epinephrine (E), and norepinephrine (NE) were analyzed. Full-Text PDF" @default.
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