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African Americans have a higher prevalence of Diabetes mellitus and associated complications. The prevalence of Vitamin D deficiency is also higher in African Americans. We report an African American veteran who was followed for a period of 10 years in the Endocrine clinic for insulin-requiring diabetes. Despite intensive, medical, nutritional and educational efforts during that period, no discernible progress was made in achieving any improvement in glycemic control. The patient appeared to be noncompliant with recommended strategies to improve glycemia. The patient was seen recently and was found to be profoundly Vitamin D deficient with a 25 (OH) Vitamin D level of 11.6 ng/ml [30-100 ng/ml]. While patient did not wish to change his insulin regimen or diabetic management, he was willing to accept Vitamin D therapy. Replacement with Vitamin D was associated with significant improvement in glycosylated hemoglobin to previously unmatched levels of glycemic control. We discuss the multiple potential mechanisms by which improved Vitamin D status may result in improved diabetes control. Given the current pandemic of Vitamin D deficiency and the plethora of potential benefits, we recommend maintaining adequate Vitamin D reserves in diabetic patients with a special emphasis on minority populations.

Significant health disparities exist between African Americans (AAs) and White Americans (WAs). The all-cause mortality rate for AAs in 2006 was 26% higher than for non-Hispanic WAs. Explanations for the disparities usually include socioeconomic status, lifestyle behaviors, social environment, and access to preventive health care services. However, several studies indicate that these factors do not account for the observed disparities. Many studies report that vitamin D has important health benefits through paracrine and autocrine mechanisms and that higher serum 25-hydroxyvitamin D (25[OH]D) levels are associated with better health outcomes. AAs have a population mean serum 25(OH)D level of 16 ng/mL, whereas WAs have a level of 26 ng/mL. From preliminary meta-analyses of serum 25(OH)D level-disease outcome from observational studies, differences in serum 25(OH)D level for AAs and WAs can explain many of the health disparities. The ratios of mortality rates for AAs to WAs for female breast cancer, colorectal cancer, cardiovascular disease, and all-cause mortality rate in 2006 were 1.34, 1.43, 1.29, and 1.26, respectively. The 25(OH)D level-disease outcome ratios for 16 ng/mL versus 26 ng/mL for the same diseases were 1.26, 1.44, 1.27, and 1.26, respectively. The close agreement between these 2 sets of numbers suggests that low serum 25(OH)D level is an important health risk for AAs. Given the widespread vitamin D deficiency in the AA population and the potential widespread health benefits that accompany adequate replacement, we believe that addressing this issue may be the single most important public health measure that can be undertaken.

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Context: GLUT4 is the predominant glucose transporter isoform expressed in fat and muscle. In GLUT4null mice, insulin-stimulated glucose uptake into muscle was diminished but not eliminated, suggesting that another insulin-sensitive system was present. Objective: This study was intended to determine whether insulin caused GLUT12 translocation in muscle. Design: Six normal volunteers had muscle biopsies before and after euglycemic insulin infusions. Setting: Infusions and biopsies were performed in an outpatient clinic. Participants: Subjects were nonobese, young adults with no family history of diabetes. Main Outcome Measures: GLUT12, GLUT4, and GLUT1 proteins were quantified in muscle biopsy fractions. Cultured myoblasts were used to determine whether GLUT12 translocation was phosphatidyl inositol-3 kinase (PI3-K)-dependent. Intervention. Insulin was infused at 40 mU/m2 • min for 3 h. Results: In human muscle, insulin caused a shift of a portion of GLUT12 from intracellular lowdensity microsomes to the plasmamembrane (PM) fraction (17% in PM at baseline, 38% in PM after insulin). Insulin increased GLUT4 in PM from 13 to 42%. GLUT1 was predominantly in the PM fractions at baseline and did not change significantly after insulin. L6 myoblasts in culture also expressed and translocated GLUT12 in response to insulin, but inhibiting PI3-K prevented the translocation of GLUT12 and GLUT4. Conclusions: Insulin causes GLUT12 to translocate from an intracellular location to the plasma membrane in normal human skeletal muscle. Translocation of GLUT12 in cultured myoblasts was dependent on activation of PI3-K. GLUT12 may have evolutionarily preceded GLUT4 and now provides redundancy to the dominant GLUT4 system in muscle.

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Objective: The authors discuss the curricular implications of a research project originally designed to evaluate the instructional strategy of using standardized patients in a psychotherapy training seminar. Methods: The original project included second-year residents enrolled in an introductory psychotherapy seminar that employed sequential meetings with standardized patients. Residents were videotaped at baseline and at 6 week intervals; these sessions were rated by outside raters, standardized patients, and the residents themselves using two rating scales designed to assess psychotherapy skill. Results of the ratings were used to assess whether the instructional strategy was effective in teaching psychotherapy. Results: Data were analyzed for group and individual effects. Results of unpaired t tests revealed that as a group resident performance did not improve. Individual effects were examined using regression analysis of individual learning plots. This analysis revealed that residents differed widely in their individual responses to this instructional technique. Conclusion: These results precipitated a realization about the curriculum. Despite initial disappointment about the apparent limitations of the technique, thoughtful analysis prompted a reinterpretation that led to residency curriculum modification.

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