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Childhood Maltreatment Is an Independent Risk Factor for Prediabetic Disturbances in Glucose Regulation
Li Li1, W Timothy Garvey2, Barbara A Gower3
1Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL, United States.
Insights
Childhood maltreatment (CM) is linked to a higher risk of prediabetes. This study found CM impairs glucose tolerance, insulin sensitivity, and beta cell function, independent of depression.
Area of Science:
- Endocrinology
- Metabolic Health
- Psychoneuroimmunology
Background:
- Childhood maltreatment (CM) is a known risk factor for obesity and depression.
- The association between CM and prediabetes, particularly its metabolic underpinnings, remains less understood.
Purpose of the Study:
- To investigate the hypothesis that CM increases the risk of prediabetes.
- To examine the impact of CM on glucose intolerance, insulin sensitivity, and beta cell function.
Main Methods:
- Assessed metabolic parameters using oral glucose tolerance tests (OGTT) in 121 adults.
- Measured CM exposure via the Childhood Trauma Questionnaire.
- Analyzed inflammatory markers and correlated them with CM severity.
Main Results:
- Individuals with CM showed a 15% higher glucose area under the OGTT curve.
- CM was associated with impaired insulin sensitivity (lower Matsuda index, higher HOMA-IR) and reduced beta cell function (lower disposition index).
- Elevated inflammatory markers (C-reactive protein, TNF-α) were observed in the CM group and correlated with CM severity.
Conclusions:
- Childhood maltreatment is significantly associated with an increased risk of prediabetes.
- CM independently contributes to glucose intolerance, impaired insulin sensitivity, and beta cell dysfunction.
- CM is identified as an independent risk factor for the development of prediabetes.
Aims:
Childhood maltreatment (CM) is shown to be associated with obesity and depression. However, the relationship of CM to prediabetic state is much less studied. We tested the hypothesis that CM increases the risk for prediabetic state due to glucose intolerance, reduced insulin sensitivity, and beta cell function.
Methods:
Oral glucose tolerance test (OGTT)-derived metabolic parameters of glucose tolerance, insulin sensitivity, and beta cell function were measured in 121 participants aged 19-60 years. CM exposure was measured using the Childhood Trauma Questionnaire. Blood samples were collected to measure the inflammatory factors.
Results:
After controlling for age, race, gender, education, and depression, about 15% higher glucose area under the OGTT curve was observed in the CM group. CM individuals also exhibited impaired insulin sensitivity manifested by the Matsuda index and homeostasis model assessment of insulin resistance, which were correlated with CM severity after adjusting for depression. CM group showed approximately 50% lower disposition index. C-reactive protein and tumor necrosis factor-α levels were greater in the CM group vs. the non-CM group, and both were correlated with CM severity (r = 0.21, 0.23, respectively, both p < 0.05). Multiple regression analyses revealed that CM contributed to reduced insulin sensitivity and lower disposition index independent of depression and visceral fat mass.
Conclusion:
These data suggest an important relationship between CM and increased risk for prediabetic state due to glucose intolerance, impaired insulin sensitivity, and beta cell function. Our findings indicate that CM appears to be an independent risk factor for developing prediabetes.
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