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      Maternal obesity: how big an impact does it have on offspring prenatally and during postnatal life?

      Author(s): ,
      Publication date Created:
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      Journal: Expert Review of Endocrinology & Metabolism
      Publisher: Informa UK Limited

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          Abstract

          Obesity is increasing at an epidemic rate in women of reproductive age. Not only does obesity during pregnancy lead to increased maternal health concerns, it is also linked to an increase in adiposity and components of the metabolic syndrome in the children and grandchildren of obese women. The potential transgenerational impact of maternal obesity on the health of future generations will undoubtedly result in increasing healthcare costs for society. This review will describe what is known about the specific impacts of maternal obesity on offspring in the human population as well as discuss how controlled animal experiments have shed light on the specific physiological mechanisms involved. Furthermore, preliminary experiments are presented describing potential dietary methods for preventing obesity-induced programming of offspring health concerns in postnatal life.

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          Toll-like receptors: critical proteins linking innate and acquired immunity.

          S Akira, K Takeda, T Kaisho (2001)
          Recognition of pathogens is mediated by a set of germline-encoded receptors that are referred to as pattern-recognition receptors (PRRs). These receptors recognize conserved molecular patterns (pathogen-associated molecular patterns), which are shared by large groups of microorganisms. Toll-like receptors (TLRs) function as the PRRs in mammals and play an essential role in the recognition of microbial components. The TLRs may also recognize endogenous ligands induced during the inflammatory response. Similar cytoplasmic domains allow TLRs to use the same signaling molecules used by the interleukin 1 receptors (IL-1Rs): these include MyD88, IL-1R--associated protein kinase and tumor necrosis factor receptor--activated factor 6. However, evidence is accumulating that the signaling pathways associated with each TLR are not identical and may, therefore, result in different biological responses.
          Article 0 comments Cited 888 times – based on 0 reviews     Review now
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            Obesity in young men after famine exposure in utero and early infancy.

            G Ravelli, Z Stein, M. Susser (1976)
            In a historical cohort study of 300,000 19-year-old men exposed to the Dutch famine of 1944-45 and examined at military induction, we tested the hypothesis that prenatal and early postnatal nutrition determines subsequent obesity. Outcomes were opposite depending on the time of exposure. During the last trimester of pregnancy and the first months of life, exposure produced significantly lower obesity rates (P less than 0.005). This result is consistent with the inference that nutritional deprivation affected a critical period of development for adipose-tissue cellularity. During the first half of pregnancy, however, exposure resulted in significantly higher obesity rates (P less than 0.0005). This observation is consistent with the inference that nutritional deprivation affected the differentiation of hypothalamic centers regulating food intake and growth, and that subsequent increased food availability produced an accumulation of excess fat in an organism growing to its predetermined maximum size.
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              Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: a study of discordant sibships.

              D Dabelea, R L Hanson, R Lindsay … (2000)
              Intrauterine exposure to diabetes is associated with an excess of diabetes and obesity in the offspring, but the effects of intrauterine exposure are confounded by genetic factors. To determine the role of the intrauterine diabetic environment per se, the prevalence of diabetes and the mean BMI were compared in siblings born before and after their mother was recognized as having diabetes. Nuclear families in which at least one sibling was born before and one after the mother was diagnosed with type 2 diabetes were selected. Consequently, the siblings born before and after differed in their exposure to diabetes in utero. A total of 58 siblings from 19 families in which at least one sibling had diabetes were examined at similar ages (within 3 years). The risk of diabetes was significantly higher in siblings born after the mother developed diabetes than in those born before the mother's diagnosis of diabetes (odds ratio 3.7, P = 0.02). In 52 families, among 183 siblings without diabetes, the mean BMI was 2.6 kg/m2 higher in offspring of diabetic than in offspring of nondiabetic pregnancies (P = 0.003). In contrast, there were no significant differences in risk of diabetes or BMI between offspring born before and after the father was diagnosed with diabetes. Intrauterine exposure to diabetes per se conveys a high risk for the development of diabetes and obesity in offspring in excess of risk attributable to genetic factors alone.
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                Author and article information

                Journal
                Title: Expert Review of Endocrinology & Metabolism
                Abbreviated Title: Expert Review of Endocrinology & Metabolism
                Publisher: Informa UK Limited
                ISSN (Print): 1744-6651
                ISSN (Electronic): 1744-8417
                Publication date Created: January 10 2014
                Publication date Created: May 2013
                Publication date (Electronic): January 10 2014
                Publication date (Print): May 2013
                Volume: 8
                Issue: 3
                Pages: 261-273
                Article
                DOI: 10.1586/eem.13.14
                PubMed ID: 30780813
                SO-VID: 64cae06d-a9fb-4327-bcdd-9e33bf532d31
                Copyright © © 2013
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