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      Activity of the Hypothalamus-Pituitary-Adrenal System and Oral Glucose Tolerance in Depressed Patients

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          We hypothesized that the activity of the hypothalamus-pituitary-adrenal system in depressed patients is related to oral glucose tolerance. In 70 moderately depressed inpatients, we measured morning saliva cortisol for 6 days and assessed oral glucose tolerance. We found glucose concentrations to be positively associated with mean morning cortisol concentrations (F<sub>3,236</sub> = 2.86, p < 0.05). Also, the ISI, a measure of insulin receptor sensitivity, was negatively associated with mean morning cortisol concentrations (r = –0.25, p < 0.04). These findings support the hypothesis that hypercortisolemia may lead to disturbed glucose utilization in depressed patients.

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          Use of the oral glucose tolerance test to assess insulin release and insulin sensitivity.

          The oral glucose tolerance test (OGTT) has often been used to evaluate apparent insulin release and insulin resistance in various clinical settings. However, because insulin sensitivity and insulin release are interdependent, to what extent they can be predicted from an OGTT is unclear. We studied insulin sensitivity using the euglycemic-hyperinsulinemic clamp and insulin release using the hyperglycemic clamp in 104 nondiabetic volunteers who had also undergone an OGTT. Demographic parameters (BMI, waist-to-hip ratio, age) and plasma glucose and insulin values from the OGTT were subjected to multiple linear regression to predict the metabolic clearance rate (MCR) of glucose, the insulin sensitivity index (ISI), and first-phase (1st PH) and second-phase (2nd PH) insulin release as measured with the respective clamps. The equations predicting MCR and ISI contained BMI, insulin (120 min), and glucose (90 min) and were highly correlated with the measured MCR (r = 0.80, P < 0.00005) and ISI (r = 0.79, P < 0.00005). The equations predicting 1st PH and 2nd PH contained insulin (0 and 30 min) and glucose (30 min) and were also highly correlated with the measured 1st PH (r = 0.78, P < 0.00005) and 2nd PH (r = 0.79, P < 0.00005). The parameters predicted by our equations correlated better with the measured parameters than homeostasis model assessment for secretion and resistance, the delta30-min insulin/delta30-min glucose ratio for secretion and insulin (120 min) for insulin resistance taken from the OGTT. We thus conclude that predicting insulin sensitivity and insulin release with reasonable accuracy from simple demographic parameters and values obtained during an OGTT is possible. The derived equations should be used in various clinical settings in which the use of clamps or the minimal model would be impractical.
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            Relationship of depression to diabetes types 1 and 2: epidemiology, biology, and treatment.

            This article reviews the rapidly accumulating literature on the relationship between mood disorders and diabetes mellitus. Recent studies have demonstrated that depression and its associated symptoms constitute a major risk factor in the development of type 2 diabetes and may accelerate the onset of diabetes complications. Since the mid-1980s, multiple longitudinal and cross-sectional studies have scrutinized the association of diabetes with depressive symptoms and major depression. Utilizing the search terms depressive disorders, psychiatry, diabetes, and pathophysiology in MEDLINE searches (1966-2003), this article reviews studies investigating pathophysiological alterations related to glucose intolerance and diabetes in depressed patients. The few randomized, controlled studies of treatment of depression in patients with diabetes are also described. Short-term treatment of depression in patients with diabetes improves their dysphoria and other signs and symptoms of depression. Future research will confirm whether response to psychotherapy and/or psychopharmacologic treatment improves glucose control, encourages compliance with diabetes treatment, and perhaps even increases longevity.
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              Prevalence of depression in adults with diabetes. An epidemiological evaluation.

              To determine the prevalence of depression in adult diabetic populations through a comprehensive literature review and to critically evaluate the methods and findings of such studies from an epidemiological perspective. A systematic review of the scientific literature revealed a total of 20 studies, 14 of which had been conducted since 1988. Nine of the studies were controlled investigations, whereas the remaining 11 studies did not contain comparison groups. The studies included both treatment and community samples. The range of the prevalence of current depression obtained from structured diagnostic interviews in diabetic samples was 8.5-27.3% (mean = 14.0%) in controlled studies and 11.0-19.9% (mean = 15.4%) in uncontrolled studies. These rates are at least three times the prevalence of major depressive disorder found in the general adult population of the U.S. Investigations using depression symptom scales corroborated these findings, as the range of clinically significant depression symptomatology in diabetic samples was 21.8-60.0% (mean = 32.4%) in controlled studies and 10.0-28.0% (mean = 19.6%) in uncontrolled studies. An increased prevalence of depression in diabetes relative to the general population is highly suggested by the literature, but biases and methodological problems commonly encountered in prevalence studies may interfere with the strength of this conclusion. An increased prevalence of depression in diabetes relative to other somatic illnesses remains unproven. The pervasive impact of depression on quality of life and its potential negative effect on diabetes management warrant recognition and treatment of the affective disorder in diabetic individuals.

                Author and article information

                S. Karger AG
                July 2005
                29 July 2005
                : 81
                : 3
                : 200-204
                aCentral Institute of Mental Health, Mannheim, and bCharité, Campus Benjamin Franklin, Department of Psychiatry, Berlin, Germany
                87003 Neuroendocrinology 2005;81:200–204
                © 2005 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 31, Pages: 5
                Original Paper


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