Low‐carbohydrate diets have been associated with significant reductions in weight and HbA1c in obese, diabetic participants who received high‐intensity lifestyle modification for 6 or 12 months. This investigation sought to determine whether comparable results to those of short‐term, intensive interventions could be achieved over a 24‐month study period using a low‐intensity intervention that approximates what is feasible in outpatient practice. A total of 144 obese, diabetic participants were randomly assigned to a low‐carbohydrate diet (<30 g/day) or to a low fat diet (≤30% of calories from fat with a deficit of 500 kcal/day). Participants were provided weekly group nutrition education sessions for the first month, and monthly sessions thereafter through the end of 24 months. Weight, HbA1c, glucose, and lipids were measured at baseline and 6, 12, and 24 months. Of the 144 enrolled participants, 68 returned for the month 24 assessment visit. Weights were retrieved from electronic medical records for an additional 57 participants (total, 125 participants) at month 24. All participants with a baseline measurement and at least one of the three other measurements were included in the mixed‐model analyses (n = 138). The low‐intensity intervention resulted in modest weight loss in both groups at month 24. At this time, participants in the low‐carbohydrate group lost 1.5 kg, compared to 0.2 kg in the low‐fat group (P = 0.147). Lipids, glycemic indexes, and dietary intake did not differ between groups at month 24 (or at months 6 or 12) (ClinicalTrials.gov number, NCT00108459).

The Clinical Islet Transplantation 07 (CIT07) protocol uses antithymocyte globulin and etanercept induction, islet culture, heparinization, and intensive insulin therapy with the same low-dose tacrolimus and sirolimus maintenance immunosuppression as in the Edmonton protocol. To determine whether CIT07 improves engrafted islet β-cell mass, our center measured β-cell secretory capacity from glucose-potentiated arginine tests at days 75 and 365 after transplantation and compared those results with the results previously achieved by our group using the Edmonton protocol and normal subjects. All subjects were insulin free, with CIT07 subjects receiving fewer islet equivalents from a median of one donor compared with two donors for Edmonton protocol subjects. The acute insulin response to glucose-potentiated arginine (AIRpot) was greater in the CIT07 protocol than in the Edmonton protocol and was less in both cohorts than in normal subjects, with similar findings for C-peptide. The CIT07 subjects who completed reassessment at day 365 exhibited increasing AIRpot by trend relative to that of day 75. These data indicate that engrafted islet β-cell mass is markedly improved with the CIT07 protocol, especially given more frequent use of single islet donors. Although several peritransplant differences may have each contributed to this improvement, the lack of deterioration in β-cell secretory capacity over time in the CIT07 protocol suggests that low-dose tacrolimus and sirolimus are not toxic to islets.

In patients with T1D experiencing problematic hypoglycemia, intrahepatic islet transplantation can lead to long-term improvement of glucose counterregulation and hypoglycemia symptom recognition, physiological effects that likely contribute to glycemic stability after transplant.

MDG may be more effective than insulin reduction for preventing exercise-induced hypoglycemia and may result in less postintervention hyperglycemia than ingestion of carbohydrate.

Real-time CGM can improve awareness and reduce the burden of problematic hypoglycemia in patients with long-standing T1D, but with only modest improvement in the endogenous glucose production response that is required to prevent or correct low blood glucose.