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LETTER TO THE EDITOR
Year : 2021  |  Volume : 19  |  Issue : 1  |  Page : 62-63

Does maternal overnutrition during pregnancy cause obesity in offspring?


Department of Public Health and Infectious Diseases, Sapienza University of Rome, Rome, Italy

Date of Submission30-Jun-2020
Date of Decision27-Jul-2020
Date of Acceptance06-Aug-2020
Date of Web Publication13-Jan-2021

Correspondence Address:
Dr. Chidiebere Emmanuel Okechukwu
Department of Public Health and Infectious Diseases, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185, Rome
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmi.cmi_108_20

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How to cite this article:
Okechukwu CE. Does maternal overnutrition during pregnancy cause obesity in offspring?. Curr Med Issues 2021;19:62-3

How to cite this URL:
Okechukwu CE. Does maternal overnutrition during pregnancy cause obesity in offspring?. Curr Med Issues [serial online] 2021 [cited 2021 Apr 20];19:62-3. Available from: https://www.cmijournal.org/text.asp?2021/19/1/62/306929



According to Chooi et al.,[1] the prevalence of obesity is more in women than men and rises with age, the global rates of overweight and obesity have augmented during the past 35 years to the level that more than one-third of the world's population is now categorized as overweight or obese, the increase in obesity worldwide may be due to interaction between dietary consumption, physical activity level, genetic, socioeconomic, and environmental factors. The developmental stage of a human is a significant phase of human formation. Obesity and other fetal programmed illness can be averted through proper health intervention, promotion, education, and awareness. Maternal exposure to adverse environmental factors can influence the epigenome, thus altering the DNA and consequently influence gene expression, which can predispose these cells and tissues to diseases across the lifespan, two main epigenetic mechanisms associated with fetal programming of diseases are DNA methylation near gene promoter regions and histone modifications, these modifications can control gene expression in an integrated and coordinated manner, for clinicians to reduce the prevalence of developmental disorders, they must begin with effective promotion of good nutrition and reduced exposures to environmental chemicals during pregnancy among women of childbearing age.[2],[3]

Based on the outcomes of animal studies, a fetus is extremely at risk of absolving surplus lipids and prenatal exposure to excess lipids may increase the risk of juvenile obesity later in life.[4] Prenatal exposure to excess energy intake, in the forms of lipids and glucose during the period of development in animals, may program an increase in food intake in the offspring. Basically, in obesity, energy intake surpasses energy expenditure, these entail changes in appetite regulation and energy expenditure.[5] A high-fat diet during fetal life could program overweight and type 2 diabetes in young adult mice.[6] However, in this scenario, there is an alteration of hypothalamic function, appetite control, and metabolic rate. Based on human studies, maternal overnutrition during pregnancy has an impact on adipocyte hypertrophy in offspring because the influx of glucose into the fetus causes an increase in fat mass.[7] Incessant weight gain during the early stage of pregnancy has been associated to high body mass index and fat mass in offspring during childhood.[8]

Leptin, a hormone secreted by fat cells in proportion to body fat mass, plays an important role in energy homeostasis by signaling the brain of deviations in both energy balance and the amount of energy deposited as fat, leptin acts in the brain as a negative feedback regulator of adiposity, by restricting energy intake and improving energy expenditure, however reduction in leptin activity promotes increased food intake, and fat accumulation, leptin's actions on energy balance are modulated through leptin receptors in hypothalamic areas, obesity can be technically defined as concomitant increase in fat mass and plasma leptin levels, signifying that obesity is a disease of leptin resistance in which high leptin levels are required to overwhelm a flaw in the leptin pathway, the leptin signaling pathway offers a potential idea on therapeutic target for the treatment of obesity.[9]

Maternal high fat feeding during pregnancy exerts deleterious effects on offspring adiposity, brain appetite regulators, and glucose lipid homeostasis. However, for effective prevention of maternal obesity-related health consequences for the offspring, there is a need to maintain weight-loss, exercise, and dietary modifications before and during pregnancy, which may impact positively on offspring metabolic health. In 2009 the US Institute of Medicine updated the gestational weight gain guidelines, despite that almost three-quarters of American women gain weight outside these guidelines [Table 1].[10] Therefore, for effective gestational weight control, these guidelines must be followed.
Table 1: 2009 US Institute of medicine recommendations for gestational weight gain during pregnancy

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In conclusion, there is a need to sustain dietary restriction policy before and during pregnancy; this can ameliorate the effects of maternal obesity on the health of offspring. Obese women can achieve weight loss before pregnancy through diet and physical activity, which in turn improves offspring metabolic phenotype. However, there is need to create awareness on the importance of a balanced diet, reduced intake of high-fat diet among women of childbearing age before and during pregnancy to improve the metabolic health of their offspring, these should be one of the primary objectives toward reducing the risk of chronic diseases in future.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Chooi YC, Ding C, Magkos F. The epidemiology of obesity. Metabolism 2019;92:6-10.  Back to cited text no. 1
    
2.
Heindel JJ, Vandenberg LN. Developmental origins of health and disease: A paradigm for understanding disease cause and prevention. Curr Opin Pediatr 2015;27:248-53.  Back to cited text no. 2
    
3.
Okechukwu CE. Prenatal exposure and fetal programming of schizophrenia. Niger J Exp Clin Biosci 2019;7:41-9.  Back to cited text no. 3
  [Full text]  
4.
McCurdy CE, Bishop JM, Williams SM, Grayson BE, Smith MS, Friedman JE, et al. Maternal high-fat diet triggers lipotoxicity in the fetal livers of nonhuman primates. J Clin Invest 2009;119:323-35.  Back to cited text no. 4
    
5.
Muhlhausler BS, Ong ZY. The fetal origins of obesity: Early origins of altered food intake. Endocr Metab Immune Disord Drug Targets 2011;11:189-97.  Back to cited text no. 5
    
6.
Gniuli D, Calcagno A, Caristo ME, Mancuso A, Macchi V, Mingrone G, et al. Effects of high-fat diet exposure during fetal life on type 2 diabetes development in the progeny. J Lipid Res 2008;49:1936-45.  Back to cited text no. 6
    
7.
Taylor PD, Poston L. Developmental programming of obesity in mammals. Exp Physiol 2007;92:287-98.  Back to cited text no. 7
    
8.
Perng W, Oken E, Dabelea D. Developmental overnutrition and obesity and type 2 diabetes in offspring. Diabetologia 2019;62:1779-88.  Back to cited text no. 8
    
9.
Guyenet SJ, Schwartz MW. Clinical review: Regulation of food intake, energy balance, and body fat mass: Implications for the pathogenesis and treatment of obesity. J Clin Endocrinol Metab 2012;97:745-55.  Back to cited text no. 9
    
10.
Goldstein RF, Abell SK, Ranasinha S, Misso ML, Boyle JA, Harrison CL, et al. Gestational weight gain across continents and ethnicity: Systematic review and meta-analysis of maternal and infant outcomes in more than one million women. BMC Med 2018;16:153.  Back to cited text no. 10
    



 
 
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