title: Maternal obesity, metabolic disease, and allostatic load.
abstract: Maternal obesity is a risk factor for many metabolic diseases for the mother, both during gestation and post partum, and for the child in later life. Obesity and pregnancy both result in altered physiological states, significantly different from the state of the non-obese, non-reproductive adult female. The concept of allostasis may be more appropriate for understanding the physiology of both pregnancy and obesity. In pregnancy these altered physiological states are adaptive, in both the evolutionary and physiological senses of the word. Obesity, however, represents a state outside of the adaptive evolutionary experience of our species. In both cases the altered physiological state derives at least in part from signals from an active endocrine organ. In obesity this is adipose tissue, and in pregnancy it is the placenta. The signaling molecules from adipose tissue and placenta all have multiple functions and can affect multiple organ systems. Placenta acts as a central regulator of metabolism for both the maternal and fetal compartments, in essence acting as a "third brain" during pregnancy. Both adipose tissue and placenta express many proinflammatory cytokines; obesity and pregnancy are states of low-grade inflammation. Both obesity and pregnancy are also states of insulin resistance, and maternal obesity is associated with fetal insulin resistance. We argue that obesity during pregnancy leads to sustained and inappropriate activation of normally adaptive regulatory circuits due in part to competing and conflicting signaling from adipose tissue and placenta. This results in allostatic load, leading to the eventual break down of regulatory mechanisms. The result is impaired metabolic function of the mother, and altered development of metabolic systems and potentially altered neural appetite circuits for the offspring.
authors.affiliation: Department of Research, American College of Obstetricians and Gynecologists, 409 12th St SW, Washington, DC 20024, United States. mpower@acog.org
authors.forename: Michael L
authors.initials: ML
authors.lastname: Power
authors.forename: Jay
authors.initials: J
authors.lastname: Schulkin
mesh_terms: D000273:Adipose Tissue / Q000502:physiology / Q000503:physiopathology; D000328:Adult; D052636:Allostasis / Q000502:physiology*; D001921:Brain / Q000502:physiology; D002648:Child; D004703:Endocrine System / Q000502:physiology / Q000503:physiopathology; D044127:Epigenesis, Genetic; D005260:Female; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007249:Inflammation / Q000503:physiopathology; D007333:Insulin Resistance; D008659:Metabolic Diseases / Q000503:physiopathology*; D009035:Mothers; D009765:Obesity / Q000503:physiopathology*; D010920:Placenta / Q000502:physiology / Q000503:physiopathology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism