Exposure to maternal diabetes in utero and offspring eating behavior: The EPOCH study

Abstract

The risk of becoming overweight among offspring exposed to gestational diabetes (GDM) in utero is two-fold higher than in the general population. The responsible mechanisms are likely multifactorial, with some evidence that GDM exposure alters brain satiety signaling, which may impact eating behavior. To better understand these effects, we investigated the relationship between GDM exposure, eating behavior, and total energy intake in 268 adolescents from the Exploring Perinatal Outcomes among Children cohort, who were exposed (n =50) or not exposed (n =217) to GDM in utero. Eating behavior was measured by the Eating in the Absence of Hunger in Children and Adolescents (EAH-C) questionnaire, which included subscale scores for Negative Affect, External Stimuli, and Fatigue/Boredom. Total energy intake (kcal/day) was derived from the Block Kid’s Food Questionnaire. The associations between GDM exposure and the outcomes of total score and each EAH-C subscale were evaluated in separate multivariable models. In addition to the main predictor, GDM, the models included a GDM-by-sex interaction term and were adjusted for important covariates. The associations between EAH-C total and subscale scores and the outcome of total energy intake were also tested in separate multivariable models. Female offspring exposed to GDM in utero (vs unexposed males and females) were more likely to continue eating beyond satiation due to feelings of boredom and fatigue (β =0.47, 95% CI: 0.11, 0.83), and in general (EAH-C total score; β =4.20, 95% CI: 0.56, 7.86) compared to unexposed males. All EAH-C subscale and total scores were significantly, positively associated with higher energy intake (p <0.05 for all, respectively). Our findings highlight the need for further investigation into the possible early life programming of eating behaviors by GDM exposure in utero.

Risks of overweight in the offspring of women with gestational diabetes at different developmental stages: A meta‐analysis with more than half a million offspring

“…The detailed characteristics of the included cohort studies are listed in Table S4. In brief, 49 identified cohort studies were conducted in 14 countries, with 12 cohort studies in the United States, [20][21][22][23][24][25][26][27][28][29][30][31] 10 in China, [32][33][34][35][36][37][38][39][40][41] 4 in Canada, [42][43][44][45] 5 in Denmark, 46-50 4 in Finland, [51][52][53][54] 3 in the United Kingdom, [55][56][57] 2 in Germany, 58,59 2 in Israel, 60,61 and 1 each in Brazil, 62 Czech Republic, 63 France, 64 India, 65 Poland, 66…”

“…67 There was one multinational study with 12 countries. 68 From our sample, 6 cohort studies reported offspring overweight and/or BMI in early childhood, 20,24,[39][40][41][42] 24 cohort studies in late childhood, [21][22][23]25,26,31,[33][34][35][36][37][38][43][44][45]53,56,58,59,[63][64][65][66][67] 15 cohort studies in the pubertal period, [27][28][29][30]32,[49][50][51][52]55,57,[60][61][62]68 and 4 cohort studies in adulthood. [46][47][48]…”

Rodent models of obesity

“…Interestingly, many studies have demonstrated the effects of an in utero HFD on offspring weight, regardless of the animal model; these observations have been replicated in human MetS [38][39][40] . The exact molecular mechanism is not well defined, although DNA methylation and histone modifications seem to play a key role 38 .…”

Long-term outcomes and potential mechanisms of offspring exposed to intrauterine hyperglycemia

“…Comparing GDM mothers treated with lifestyle or antidiabetic agents with their non-diabetic counterparts, the linear regression analysis showed that O-GDM mothers developed their neuropsychiatric conditions at a younger age ( 94 ). Exposure to diabetes mellitus in utero also led to eating disorders in the offspring at adolescence ( 96 , 97 ). The hypothalamic blood flow in response to glucose in children of GDM mothers was obviously higher than control, combined with hypothalamic sensitivity to glucose stimulation ( 98 ).…”