Alterations in Insulin Levels in Adults with Prenatal Alcohol Exposure

Abstract

Objective Evidence suggests that prenatal alcohol exposure (PAE) may adversely impact insulin production and signaling but there is limited information on the range of these effects and their future health consequences. Method A prospective cohort of predominantly African‐American individuals identified while in utero and followed into adulthood were used to evaluate differences in various indicators of diabetes, including fasting plasma glucose, hemoglobin A1c (HbA1c), and insulin levels. The homeostatic model assessment of insulin resistance (HOMA‐IR) was also computed. Body mass index (BMI) was calculated and normal defined as < 25 kg/m2. Participants were categorized as having PAE (n = 39) if their mothers drank at least 1 ounce of absolute alcohol per week or more during the 1st trimester of pregnancy and as Controls (n = 22) if their mothers reported abstaining from alcohol consumption during pregnancy. Results Mean age of the sample was 36.0 ± 1.5 years. Indices of glucose metabolism, including fasting plasma glucose and hemoglobin A1c levels, did not vary by group status but insulin levels and HOMA‐IR values varied by group status and BMI level. PAE individuals with a normal BMI had lower insulin levels than Controls. However, in PAE subjects, there was a steeper increase in insulin levels relative to their BMI than in Control subjects. A cluster of 5 PAE cases had low levels of insulin and 4 of the 5 had severe cognitive impairment. Conclusions The bidirectional effects on insulin level and insulin resistance associated with PAE may indicate differential rates of diabetes disease impact or differential PAE impact in the brain and peripheral areas involved in insulin production and signaling. These alterations may contribute to the metabolic disease risk associated with PAE.

Aging-Related Behavioral, Adiposity, and Glucose Impairments and Their Association following Prenatal Alcohol Exposure in the C57BL/6J Mouse

“…Castells et al [ 13 ] described elevated plasma insulin in an oral glucose tolerance test in children with fetal alcohol syndrome, suggesting they had greater insulin resistance. In contrast, a cohort of mostly African Americans with FASD (mean age 36 years) had lower mean BMIs and no difference in their diabetic indicators (fasting glucose, HOMA-IR); although, they had a steeper slope when BMI was plotted against fasting insulin [ 14 ]. Although children diagnosed with FASD are more typically lean or even underweight, likely because small-for-age is part of the diagnostic criteria [ 1 ], elevated adiposity is more frequently observed in females, but not males, starting around the time of adolescence [ 12 , 15 , 16 , 17 , 18 ].…”

Fetal Alcohol Spectrum Disorders: Awareness to Insight in Just 50 Years

“… 58 Premature death and increased prevalence of metabolic, immune, and cardiovascular disorders have been reported in informal surveys of adults with FASD 56 as well as in epidemiological studies. 55 , 59 For example, studies in human cohorts and zebrafish indicate that PAE induces elements of metabolic syndrome in adults by modifying developmental programs for hepatic and adipose tissue embryogenesis. 60 Further research will be important to delineate the full range of human diseases associated with PAE to allow for earlier detection and intervention.…”

Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood

“…One study reported that individuals diagnosed with FASDs have a higher mortality rate at every age range beginning in the late teenage and young adulthood [123]. This increase in mortality rate is contributable in part to systemic diseases, such as metabolic, cardiovascular, endocrine, renal, and respiratory disease, which are the second leading cause of death at 25% after mental health/drug overdoses at 27% [123][124][125][126][127]. A DOHaD approach to understanding this increase in mortality and systemic disease reveals the pathogenic underpinnings in individuals with FASDs and the long-term effects of the toxic and teratogenic mechanisms of PAE (Figure 3).…”