Edited by Helaine E. Resnick, PhD, MPH

In this issue of Diabetes Care, Luijf et al. (p. 3882) demonstrate meaningful progress in closed-loop control of type 1 diabetes using currently available insulin pumps and sensors. Although technologies that automate glucose monitoring and insulin administration have been available for some time, concerns about the accuracy of continuous glucose monitoring data that these systems generate have created challenges for the development of user-friendly, closed-loop systems for safe and effective glucose control. Currently, there are a number of algorithms that use patient characteristics and data from insulin pumps to manage glucose. But the relative merits of these algorithms are not well understood in terms of their impact on basic end points such as time spent in target and time in hypo- and hyperglycemia. Addressing these questions, the new report compares the performance of two closed-loop algorithms—the iAP and CAM—to patient self-control (open loop) in a sample of 48 patients from 6 clinical centers. Unlike previous studies, these patients underwent a full day of closed-loop control, including meals. Eight patients were enrolled at each center, with some centers being more experienced with these experimental protocols than others. Results showed that the percent of time patients spent in target glucose ranges was similar among the three groups: 58.3, 59.2, and 62.6% among CAM, iAP, and open-loop participants, respectively. There was an interesting trade-off between average glucose levels and percent of time in hypoglycemia, with the closed-loop participants having less favorable average glucose levels but more favorable hypoglycemia profiles. Average glucose was 8.26, 8.15, and 7.19 mmol/L in the CAM, iAP, and open-loop participants, respectively, while percent of time in hypoglycemia was 2.0, 2.1, and 6.4% in the same groups. In addition to the overall conclusion that both the iAP and CAM algorithms provide safe glycemic control, another import finding of this study was that relatively inexperienced clinical centers could successfully conduct closed-loop protocols—an important consideration for future studies that will require larger numbers of participants to assess the longer-term benefits of closed-loop control as these approaches move toward broader application. — Helaine E. Resnick, PhD, MPH

Luijf et al. Day and night closed-loop control in adults with type 1 diabetes: a comparison of two closed-loop algorithms driving continuous subcutaneous insulin infusion versus patient self-management. Diabetes Care 2013;36:3882–3887

Although there is often a feeling that among children and young adults, a diagnosis of type 2 diabetes is “bad, but less bad” than a diagnosis of type 1 diabetes, the findings of a new report in this issue of Diabetes Care (p. 3863) do not support this idea. In an effort to compare long-term outcomes across the two major types of diabetes, investigators examined a database with more than 20 years of historical data on adolescents and young adults with type 1 and type 2 diabetes. All people included in the study had diabetes onset between the ages of 15 and 30 years. The opportunity to age-match across the two diabetes groups helped investigators isolate the contribution of diabetes type to both mortality and large and small vessel outcomes: this design greatly facilitated controlling for the potentially confounding effects of age and diabetes duration that have plagued other studies. The investigators showed that over 20 years, the risk of all-cause mortality in the type 2 diabetic group was twice that in the type 1 diabetic group, and the data also indicated that death occurred at younger ages among people with type 2 diabetes, and at a point when these individuals had diabetes for a significantly shorter period of time than their type 1 counterparts. Interestingly, although glycemic control was similar across the two groups, the type 2 diabetic group still had less favorable cardiovascular disease risk profiles as well as more albuminuria and worse neuropathy scores. Taken together, the authors concluded that type 2 diabetes is a more “lethal phenotype” than type 1 diabetes. If so, the findings of this new report do not bode well for the increasingly large numbers of adolescents and young adults who are being diagnosed with diabetes at ever younger ages. — Helaine E. Resnick, PhD, MPH

Constantino et al. Long-term complications and mortality in young-onset diabetes: type 2 diabetes is more hazardous and lethal than type 1 diabetes. Diabetes Care 2013;36:3863–3869

A report in this issue of Diabetes Care (p. 4036) sheds light on the underlying link between type 2 diabetes and cognitive dysfunction. It has been known for some time that type 2 diabetes is associated with increased risk of cognitive decline and Alzheimer disease, and that MRI images of diabetic brains frequently show infarcts and microbleeds. People with type 2 diabetes also have lower hippocampal and total brain volumes. Despite these observations, the question of whether the cognitive impairment that is observed in diabetes results from cerebrovascular lesions or neurodegeneration remains unanswered. New data from Moran et al. suggest that hippocampal and total gray matter volumes are sources of the decreased cognitive function observed in diabetes. The investigators conducted extensive cognitive testing and neuroimaging on more than 700 people with and without type 2 diabetes, with a focus on the regional distribution of brain atrophy and its association with various aspects of cognitive function. The results showed that diabetic subjects had significantly lower total gray, white, and hippocampal volumes and more cerebral infarcts. As expected, initial regression analyses indicated that people with type 2 diabetes had less favorable function across a number of cognitive batteries relative to their nondiabetic counterparts. However, the magnitude of the associations between type 2 diabetes and these functional outcomes was reduced by about half when hippocampal and total gray volumes were included in the model—a finding that suggests brain atrophy in these regions is responsible for the diminished cognitive function observed in diabetes. Importantly, although cerebral infarcts were also more common in the diabetic participants, adjustment for infarcts in the regression models did not change the association between diabetes and cognitive function. This suggests that these lesions do not play a role in diabetes-associated cognitive impairment. Another key observation from the new study is that the pattern of brain atrophy that is observed in type 2 diabetes is similar to the one in early Alzheimer disease. Taken in the larger context of the association between type 2 diabetes and Alzheimer disease, the new findings in this issue of the journal may provide insight into the brain morphology that underpins a potential link between abnormalities of glucose metabolism and development of Alzheimer disease. — Helaine E. Resnick, PhD, MPH

Moran et al. Brain atrophy in type 2 diabetes: regional distribution and influence on cognition. Diabetes Care 2013;36:4036–4042

Probability map of location of gray matter atrophy attributable to type 2 diabetes.

Probability map of location of gray matter atrophy attributable to type 2 diabetes.

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Data in this issue of Diabetes Care (p. 3897) suggest the need to reconsider approaches to postprandial insulin delivery in children with intensively treated type 1 diabetes. Although prandial insulin dosing is currently based on the carbohydrate content of the meal, supplemental insulin has been suggested for meals that are high in fat because of the glucose excursions that have been observed with higher-fat meals. However, new dosing algorithms that take both fat and protein into account have been associated with increased hypoglycemia in children. Taken together, these observations suggest the need to better understand the impact of various combinations of fat and protein on postprandial glucose in children with type 1 diabetes. Responding to this need, Smart et al. studied 33 children aged 8–17 years who were intensively treated for type 1 diabetes. The new report focuses on the impact of four test breakfasts, each of which had the same carbohydrate content, but varied in their protein and fat content (high/low). Children were given an individualized insulin dose, and postprandial glucose was examined for 5 h after administration of the test meals to understand both the short- and long-term impact of the nutrient content. Results showed higher glucose excursions from 180 min in meals that were high in protein, regardless of fat content. Notably, meals that were high in both fat and protein showed the most pronounced excursions relative to all other meals, and these occurred from 180 to 300 min after meal administration. The authors point out that their findings have a direct impact on clinical translation because the meals used in these experiments are typical of those consumed by children. Against this backdrop, the late, sustained impact of the high-protein/high-fat meals may indicate the need to rethink strategies for insulin dosing in intensively treated children with type 1 diabetes. — Helaine E. Resnick, PhD, MPH

Smart et al. Both dietary protein and fat increase postprandial glucose excursions in children with type 1 diabetes, and the effect is additive. Diabetes Care 2013;36:3897–3902

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