Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
16 - The developmental environment and the endocrine pancreas
Published online by Cambridge University Press: 08 August 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- 1 The developmental origins of health and disease: an overview
- 2 The ‘developmental origins’ hypothesis: epidemiology
- 3 The conceptual basis for the developmental origins of health and disease
- 4 The periconceptional and embryonic period
- 5 Epigenetic mechanisms
- 6 A mitochondrial component of developmental programming
- 7 Role of exposure to environmental chemicals in developmental origins of health and disease
- 8 Maternal nutrition and fetal growth and development
- 9 Placental mechanisms and developmental origins of health and disease
- 10 Control of fetal metabolism: relevance to developmental origins of health and disease
- 11 Lipid metabolism: relevance to developmental origins of health and disease
- 12 Prenatal hypoxia: relevance to developmental origins of health and disease
- 13 The fetal hypothalamic–pituitary–adrenal axis: relevance to developmental origins of health and disease
- 14 Perinatal influences on the endocrine and metabolic axes during childhood
- 15 Patterns of growth: relevance to developmental origins of health and disease
- 16 The developmental environment and the endocrine pancreas
- 17 The developmental environment and insulin resistance
- 18 The developmental environment and the development of obesity
- 19 The developmental environment and its role in the metabolic syndrome
- 20 Programming the cardiovascular system
- 21 The role of vascular dysfunction in developmental origins of health and disease: evidence from human and animal studies
- 22 The developmental environment and atherogenesis
- 23 The developmental environment, renal function and disease
- 24 The developmental environment: effect on fluid and electrolyte homeostasis
- 25 The developmental environment: effects on lung structure and function
- 26 Developmental origins of asthma and related allergic disorders
- 27 The developmental environment: influences on subsequent cognitive function and behaviour
- 28 The developmental environment and the origins of neurological disorders
- 29 The developmental environment: clinical perspectives on effects on the musculoskeletal system
- 30 The developmental environment: experimental perspectives on skeletal development
- 31 The developmental environment and the early origins of cancer
- 32 The developmental environment: implications for ageing and life span
- 33 Developmental origins of health and disease: implications for primary intervention for cardiovascular and metabolic disease
- 34 Developmental origins of health and disease: public-health perspectives
- 35 Developmental origins of health and disease: implications for developing countries
- 36 Developmental origins of health and disease: ethical and social considerations
- 37 Past obstacles and future promise
- Index
- References
Summary
Introduction
The intrauterine environment is the first to which the conceptus is exposed and it is strongly influenced by the mother's health. In this chapter we will focus on the development of the endocrine pancreas. A disturbed intrauterine metabolic milieu would contribute to inappropriate β-cell ontogeny, resulting in a population of β cells that does not adequately cope with metabolic or oxidative stress later in life. This hypothesis obviously cannot be verified in humans; therefore various animal models have been established.
Development of the endocrine pancreas in the rodent
The development of the pancreas in rodents shows similarities to that in humans. However, while fetal β cells are functioning as true endocrine cells at the end of the first trimester in humans (Piper et al. 2004), this occurs only during the last third of gestation in the rat. The development of the pancreas is a fascinating event, starting from a pool of common progenitor cells (multipotent endodermal progenitors) which will be committed into the endocrine or exocrine cell lineages or become duct cells. Then, within the endocrine compartment, the cells will have to further differentiate into α, β, δ or PP cells producing glucagon, insulin, somatostatin or the pancreatic polypeptide respectively. This is regulated by the expression of distinct genes, under the control of a hierarchy of various specific networks of transcription factors.
- Type
- Chapter
- Information
- Developmental Origins of Health and Disease , pp. 233 - 243Publisher: Cambridge University PressPrint publication year: 2006
References
, and (1990). Maternal diabetes during pregnancy: consequences for the offspring. Diabetes Metab. Rev., 16, 147–67.CrossRefGoogle Scholar
and (2001). Type 1 diabetes: new perspectives on disease pathogenesis and treatment. Lancet, 358, 221–9.CrossRefGoogle ScholarPubMed
, ., , , and (2002). Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy. Am. J. Physiol. Regul. Integr. Comp. Physiol., 283, R623–30.CrossRefGoogle ScholarPubMed
, , and (1999). Age-dependant inability of the endocrine pancreas to adapt to pregnancy: a long term consequence of perinatal malnutrition in the rat. Endocrinology, 40, 4208–13.CrossRefGoogle Scholar
, , , and (2001). Glucocorticoids impair fetal β-cell development in rat. Am. J. Physiol. Endocrinol. Metab., 281, E592–9.CrossRefGoogle Scholar
, , and (2002). Endocrine pancreas development is altered in fetuses from rats previously showing intra-uterine growth retardation in response to malnutrition. Diabetologia, 45, 394–401.CrossRefGoogle Scholar
, and (2002). Gestational diabetes leads to the development of diabetes in adulthood in the rat. Diabetes, 51, 1499–506.CrossRefGoogle ScholarPubMed
and (1976). Metabolic adaptation to pregnancy shown by increased biosynthesis of insulin islets of Langerhans isolated from pregnant rats. Nature, 262, 501–2.CrossRefGoogle Scholar
, , et al. (2003). Evaluation of the new ADA and WHO criteria for classification of diabetes mellitus in young adult people (15–34 yrs) in the Diabetes Incidence Study in Sweden (DISS). Diabetologia, 46, 173–81.CrossRefGoogle Scholar
, , et al. (2002). Taurine supplementation to a low protein diet during fetal and early postnatal life restores a normal proliferation and apoptosis of rat pancreatic islets. Diabetologia, 45, 856–66.CrossRefGoogle ScholarPubMed
, , , and (2003). Taurine supplementation of a low protein diet fed to rat dams normalized the vascularization of the fetal endocrine pancreas. J. Nutr., 133, 2820–5.CrossRefGoogle Scholar
, , and (2001). A protein-restricted diet during pregnancy alters in vitro insulin secretion from islets of fetal Wistar rat. J. Nutr., 131, 1555–9.CrossRefGoogle Scholar
, , et al. (1988). Islet amyloid, increased A-cells, reduced B-cell and exocrine fibrosis: quantitative changes in the pancreas in type 2 diabetes. Diabetes Res., 9, 151–9.Google ScholarPubMed
, and (2000). Effect of diabetes in pregnancy on offspring: follow-up research in the Pima Indians. J. Matern. Fetal. Med., 9, 83–8.Google ScholarPubMed
, , , and (1991). Islet function in offspring of mothers on low-protein diet during gestation. Diabetes, 40, 115–20.CrossRefGoogle ScholarPubMed
, , and (1978). Effect of glucose and amino acids on fetal rat pancreatic growth and insulin secretion in vitro. J. Endocrinol., 77, 241–8.CrossRefGoogle Scholar
, , and (2004). Adult pancreatic beta cells are formed by self-duplication rather than stem-cell differentiation. Nature, 429, 41–6.CrossRefGoogle ScholarPubMed
(2001). Factors controlling pancreatic cell differentiation and function. Diabetologia, 44, 1071–9.CrossRefGoogle ScholarPubMed
(1980). Banting Lecture 1980. Of pregnancy and progeny. Diabetes, 29, 1023–35.CrossRefGoogle ScholarPubMed
, and (1997). In utero undernutrition impairs rat β-cell development. Diabetologia, 40, 1231–4.CrossRefGoogle ScholarPubMed
, and (1998). Beta-cell mass and proliferation following late fetal and early postnatal malnutrition in the rat. Diabetologia, 34, 373–84.Google Scholar
, and (2001). Key events of pancreas formation are triggered in gut endoderm by ectopic expression of pancreatic regulatory genes. Genes Dev., 15, 44–54.CrossRefGoogle ScholarPubMed
, , and (2001). No decrease of the beta-cell mass in type 2 diabetic patients. Diabetes, 50 (Suppl. 1), S188.CrossRefGoogle ScholarPubMed
, and (1998). Notochord repression of endodermal Sonic hedgehog permits pancreas development. Genes Dev., 12, 1705–13.CrossRefGoogle ScholarPubMed
, , and (1993). Interactions of glucose, insulin like growth factors (IGFs) and IGF binding proteins in the regulation of DNA synthesis by isolated fetal rat islets of Langerhans. J. Endocrinol., 138, 401–12.CrossRefGoogle ScholarPubMed
, and (1991). Evidence for an insulin resistance in the adult offspring of pregnant streptozotocin-diabetic rats. Diabetologia, 34, 81–5.CrossRefGoogle ScholarPubMed
(1994). The role of reduced glucose transporter content and glucose metabolism in the immature secretory responses of fetal rat pancreatic islets. Diabetologia, 37, 134–40.CrossRefGoogle ScholarPubMed
(1998). Type 2 diabetes: when insulin secretion fails to compensate for insulin resistance. Cell, 92, 593–6.CrossRefGoogle ScholarPubMed
, and (1978). The endocrine pancreas of the fetus from diabetic pregnant rat. Diabetologia, 15, 387–93.CrossRefGoogle ScholarPubMed
, and (2001). Induction of pancreatic differentiation by signals from blood vessels. Science, 294, 564–7.CrossRefGoogle ScholarPubMed
, , , and (2001). Maternal undernutrition during late gestation induces fetal overexposure to glucocorticoids and intrauterine growth retardation, and disturbs the hypothalamo-pituitary adrenal axis in the newborn rat. Endocrinology, 142, 1692–702.CrossRefGoogle Scholar
, , , and (2001). Intraurerine low protein diet increases fetal β cell sensitivity to NO and IL-1-β: the protective role of taurine. J. Endocrinol., 171, 299–308.CrossRefGoogle ScholarPubMed
, , and (2004). Effect of maternal low protein diet and taurine on the vulnerability of Wistar rat islets to cytokines. Diabetologia, 7, 669–75.Google Scholar
, , and (1998). Apoptosis in the pancreatic islet cells of the neonatal rat is associated with a reduced expression of insulin-like growth factor II that may act as a survival factor. Endocrinology, 139, 2994–3004.CrossRefGoogle ScholarPubMed
, , et al. (1999). A low protein diet alters the balance of islet cell replication and apoptosis in the fetal and neonatal rat and is associated with a reduced pancreatic expression of insulin like growth factor II. Endocrinology, 140, 4861–73.CrossRefGoogle ScholarPubMed
, , et al. (2004). Beta cell differentiation during human pancreas developmentJ. Endocrinol., 181, 11–23.CrossRefGoogle ScholarPubMed
and (2001a). Intergenerational effects of adverse intrauterine environment on perturbation of glucose metabolism. Twin Res., 4, 406–11.CrossRefGoogle Scholar
Reusens, B. and Remacle, C. (2001b). Effects of maternal nutrition and metabolism on the developing endocrine pancreas. In Fetal Origins of Cardiovascular and Lung Disease (ed. ). New York, NY: Marcel Dekker, pp. 339–58.Google Scholar
Reusens, B., Dahri, S., Snoeck, A., Bennis-Taleb, N., Remacle, C. and Hoet, J. J. (1995). Long-term consequences of diabetes and its complications may have a fetal origin: experimental evidence. In Diabetes (ed. ). New York, NY: Raven Press, pp. 187–98.Google Scholar
Reusens, B., Hoet, J. J. and Remacle, C. (2000). Anatomy, developmental biology and pathology of the pancreatic islets. In Endocrinology (ed. et al.). Philadelphia, PA: Saunders, pp. 5024–35.
, , and (1984). Cell proliferation in pancreatic islets of rat fetus and neonates from normal and diabetic mothers: an in vitro and in vivo study. Horm. Metab. Res., 16, 565–71.CrossRefGoogle Scholar
, , and (1997). Apoptosis participates in the remodelling of the endocrine pancreas in the neonatal rat. Endocrinology, 138, 1736–41.CrossRefGoogle Scholar
, , and (1990). Effect of a low protein diet during pregnancy on the fetal rat endocrine pancreas. Biol. Neonate, 57, 107–18.CrossRefGoogle ScholarPubMed
and (1997). Adaptation of islets of Langerhans to pregnancy: beta-cell growth, enhanced insulin secretion and the role of lactogenic hormones. Horm. Metab. Res., 29, 301–7.CrossRefGoogle ScholarPubMed
, , and (2003). Neonatal Exendin-4 prevents the development of diabetes in the intrauterine growth retarded rat. Diabetes, 52, 734–40.CrossRefGoogle ScholarPubMed
, , , , and (2000). Perspectives in diabetes. Neonatal β-cell apoptosis: a trigger for autoimmune diabetes. Diabetes, 49, 1–7.CrossRefGoogle Scholar
, , et al. (1997). UKPDS 25: autoantibodies to islet cell cytoplasm and glutamic acid decarboxylase for prediction of insulin requirement in type 2 diabetes. Lancet, 350, 1288–93.CrossRefGoogle ScholarPubMed
, , , and (2000). Fetal origin of hyperphagia, obesity and hypertension and its postnatal amplification by hypercaloric nutrition. Am. J. Physiol. Endocrinol. Metab., 279, E83–7.CrossRefGoogle Scholar
, and (2003). Gene expression cascades in pancreas development. Mech. Dev., 120, 65–80.CrossRefGoogle Scholar
and (1966). Cellular response in rats during malnutrition at various ages. J. Nutr., 89, 300–6.CrossRefGoogle ScholarPubMed
- 1
- Cited by