for the Wireless Innovation for Seniors With Diabetes Mellitus (WISDM) Study Group IMPORTANCE Continuous glucose monitoring (CGM) provides real-time assessment of glucose levels and may be beneficial in reducing hypoglycemia in older adults with type 1 diabetes. OBJECTIVE To determine whether CGM is effective in reducing hypoglycemia compared with standard blood glucose monitoring (BGM) in older adults with type 1 diabetes. DESIGN, SETTING, AND PARTICIPANTS Randomized clinical trial conducted at 22 endocrinology practices in the United States among 203 adults at least 60 years of age with type 1 diabetes. INTERVENTIONS Participants were randomly assigned in a 1:1 ratio to use CGM (n = 103) or standard BGM (n = 100). MAIN OUTCOMES AND MEASURESThe primary outcome was CGM-measured percentage of time that sensor glucose values were less than 70 mg/dL during 6 months of follow-up. There were 31 prespecified secondary outcomes, including additional CGM metrics for hypoglycemia, hyperglycemia, and glucose control; hemoglobin A 1c (HbA 1c ); and cognition and patient-reported outcomes, with adjustment for multiple comparisons to control for false-discovery rate. RESULTSOf the 203 participants (median age, 68 [interquartile range {IQR}, 65-71] years; median type 1 diabetes duration, 36 [IQR, years; 52% female; 53% insulin pump use; mean HbA 1c , 7.5% [SD, 0.9%]), 83% used CGM at least 6 days per week during month 6. Median time with glucose levels less than 70 mg/dL was 5.1% (73 minutes per day) at baseline and 2.7% (39 minutes per day) during follow-up in the CGM group vs 4.7% (68 minutes per day) and 4.9% (70 minutes per day), respectively, in the standard BGM group (adjusted treatment difference, −1.9% (−27 minutes per day); 95% CI, −2.8% to −1.1% [−40 to −16 minutes per day]; P <.001). Of the 31 prespecified secondary end points, there were statistically significant differences for all 9 CGM metrics, 6 of 7 HbA 1c outcomes, and none of the 15 cognitive and patient-reported outcomes. Mean HbA 1c decreased in the CGM group compared with the standard BGM group (adjusted group difference, −0.3%; 95% CI, −0.4% to −0.1%; P <.001). The most commonly reported adverse events using CGM and standard BGM, respectively, were severe hypoglycemia (1 and 10), fractures (5 and 1), falls (4 and 3), and emergency department visits (6 and 8).CONCLUSIONS AND RELEVANCE Among adults aged 60 years or older with type 1 diabetes, continuous glucose monitoring compared with standard blood glucose monitoring resulted in a small but statistically significant improvement in hypoglycemia over 6 months. Further research is needed to understand the long-term clinical benefit.

Atypical antipsychotic (AAP) medications that have revolutionized the treatment of mental illness have become stigmatized by metabolic side effects, including obesity and diabetes. It remains controversial whether the defects are treatment induced or disease related. Although the mechanisms underlying these metabolic defects are not understood, it is assumed that the initiating pathophysiology is weight gain, secondary to centrally mediated increases in appetite. To determine if the AAPs have detrimental metabolic effects independent of weight gain or psychiatric disease, we administered olanzapine, aripiprazole, or placebo for 9 days to healthy subjects (n = 10, each group) under controlled in-patient conditions while maintaining activity levels. Prior to and after the interventions, we conducted a meal challenge and a euglycemic-hyperinsulinemic clamp to evaluate insulin sensitivity and glucose disposal. We found that olanzapine, an AAP highly associated with weight gain, causes significant elevations in postprandial insulin, glucagon-like peptide 1 (GLP-1), and glucagon coincident with insulin resistance compared with placebo. Aripiprazole, an AAP considered metabolically sparing, induces insulin resistance but has no effect on postprandial hormones. Importantly, the metabolic changes occur in the absence of weight gain, increases in food intake and hunger, or psychiatric disease, suggesting that AAPs exert direct effects on tissues independent of mechanisms regulating eating behavior.

Abstract Context Minority young adults (YA) currently represent the largest growing population with type 1 diabetes (T1D) and experience very poor outcomes. Modifiable drivers of disparities need to be identified, but are not well-studied. Objective To describe racial-ethnic disparities among YA with T1D and identify drivers of glycemic disparity other than socioeconomic status (SES). Design Cross-sectional multicenter collection of patient and chart-reported variables, including SES, social determinants of health, and diabetes-specific factors, with comparison between non-Hispanic White, non-Hispanic Black, and Hispanic YA and multilevel modeling to identify variables that account for glycemic disparity apart from SES. Setting Six diabetes centers across the United States. Participants A total of 300 YA with T1D (18-28 years: 33% non-Hispanic White, 32% non-Hispanic Black, and 34% Hispanic). Main Outcome Racial-ethnic disparity in HbA1c levels. Results Non-Hispanic Black and Hispanic YA had lower SES, higher HbA1c levels, and much lower diabetes technology use than non-Hispanic White YA (P &lt; 0.001). Non-Hispanic Black YA differed from Hispanic, reporting higher diabetes distress and lower self-management (P &lt; 0.001). After accounting for SES, differences in HbA1c levels disappeared between non-Hispanic White and Hispanic YA, whereas they remained for non-Hispanic Black YA (+ 2.26% [24 mmol/mol], P &lt; 0.001). Diabetes technology use, diabetes distress, and disease self-management accounted for a significant portion of the remaining non-Hispanic Black–White glycemic disparity. Conclusion This study demonstrated large racial-ethnic inequity in YA with T1D, especially among non-Hispanic Black participants. Our findings reveal key opportunities for clinicians to potentially mitigate glycemic disparity in minority YA by promoting diabetes technology use, connecting with social programs, and tailoring support for disease self-management and diabetes distress to account for social contextual factors.

We used intravenous arginine with measurements of insulin, C-peptide, and glucagon to examine β-cell and α-cell survival and function in a group of 10 chronic pancreatitis recipients 1–8 years after total pancreatectomy and autoislet transplantation. Insulin and C-peptide responses correlated robustly with the number of islets transplanted (correlation coefficients range 0.81–0.91; P < 0.01–0.001). Since a wide range of islets were transplanted, we normalized the insulin and C-peptide responses to the number of islets transplanted in each recipient for comparison with responses in normal subjects. No significant differences were observed in terms of magnitude and timing of hormone release in the two groups. Three recipients had a portion of the autoislets placed within their peritoneal cavities, which appeared to be functioning normally up to 7 years posttransplant. Glucagon responses to arginine were normally timed and normally suppressed by intravenous glucose infusion. These findings indicate that arginine stimulation testing may be a means of assessing the numbers of native islets available in autologous islet transplant candidates and is a means of following posttransplant α- and β-cell function and survival.

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