Emotional Regulation and Diabetes Distress in Adults With Type 1 and Type 2 Diabetes.

OBJECTIVE: To explore the correlates of diabetes-related distress (DD) with psychometrically valid assessments of emotional regulation in individuals with type 1 and type 2 diabetes. RESEARCH DESIGN AND METHODS: Adults with diabetes (n = 298) were assessed for psychological issues possibly associated with diabetes and were further evaluated with measures of negative emotional experience (ER-Exp) and skill at regulating such experiences (ER-Skill) and measures of DD, perceived psychosocial stress, diabetes literacy, and diabetes self-care. RESULTS: ER-Exp was directly related to DD, while ER-Skill was inversely related to DD. Together, these ER variables displayed a medium-size relationship (ß = 0.45) with DD. Inclusion of variables related to diabetes self-care and perceived psychosocial stress was associated with only an 18% reduction (i.e., ß = 0.45 to ß = 0.38) in the strength of this relationship, while the magnitude of relationships between DD and perceived psychosocial stress (ß = 0.15) and diabetes self-care (ß = -0.09) was relatively small. CONCLUSIONS: These data suggest that DD is meaningfully linked with negative emotionality, and skill at regulating such emotions, in adults with diabetes. This relationship appears to be stronger than that between DD and perceived psychological stress or diabetes self-care. If so, DD (and possibly A1C) may be improved in those with diabetes and difficulties with negative emotionality.

HbA1c levels as a function of emotional regulation and emotional intelligence in patients with type 2 diabetes.

AIMS: Understanding the role of emotion in glycemic control may be critical for the long-term treatment of patients with type 2 diabetes (T2D). In this study we investigated the relationship between measures of emotional regulation and emotional intelligence and HbA1c levels in adult patients with T2 diabetes. METHODS: 100 adult patients with T2 diabetes completed assessments of emotional regulation (i.e., affect intensity/lability) and emotional intelligence and were then correlated with HbA1c levels with several relevant covariates. RESULTS: HbA1c levels were significantly associated with affect intensity (AI: r=.24, p=.018) and with emotional intelligence (EI: r=-.29, p=.004), but not affect lability. These results were the same even after adding income, state depression scores, insulin-dependent status, serum cholesterol, diabetes literacy and self-care as covariates (AI: ß=.33, p=.001; EI: ß=-.31, p=.002). Diabetes self-care, but not diabetes literacy, was also associated with HbA1c levels (ß=-.29, p=.003). CONCLUSIONS: These data suggest that aspects of emotional regulation and emotional intelligence play a role in glycemic control in adult patients with T2 diabetes and do so even in the context of several variables relevant to diabetes. If so, interventions that can reduce affect intensity and/or increase emotional intelligence may represent a new strategy in the glycemic control of adult patients with T2 diabetes.

Mechanisms of glucose sensing in the pancreatic ß-cell: A computational systems-based analysis.

Pancreatic ß-cells respond to rising blood glucose by increasing oxidative metabolism, leading to an increased ATP/ADP ratio in the cytoplasm with a subsequent influx of calcium and the eventual secretion of insulin. The mechanisms of glucose sensing in the pancreatic ß-cell involve the coupling of cytoplasmic and mitochondrial processes. Our analysis, based on mathematical models of data from multiple sources has implications for ß-cell function and the treatment of type 2 diabetes (Fridlyand and Philipson, 2010). This ß-cell glucose response model correctly predicts changes in the ATP/ADP ratio, cytoplasmic and mitochondrial calcium levels, and other metabolic parameters in response to alterations in substrate delivery at steady-state and during cytoplasmic calcium oscillations. Here we consider how peculiarities of ß-cell pathways that result in dysfunction can be a consequence of specific mechanisms of glucose sensitivity, using our computational systems-based analysis. We found that the mitochondrial membrane potential must be relatively low in ß-cells compared with other cell types to permit precise mitochondrial regulation of the cytoplasmic ATP/ADP ratio. This key difference may follow from a relative reduction in cellular respiratory activity. Our analysis additionally demonstrates how activity of lactate dehydrogenase, uncoupling proteins, and the redox shuttles all working in concert can regulate ß-cell function. We further show that a decreased mitochondrial membrane potential may lead to a low rate of production of reactive oxygen species in ß-cells under physiological conditions. This computational systems analysis aids in providing a more complete understanding of the complex process of ß-cell glucose sensing.