Dinneen, Seán F.

Abstract Aim This study aims to assess the treatment burden and health‐related quality of life (HRQoL) in young adults with type 1 diabetes (T1D). Methods Online survey on experienced treatment burden (Treatment Burden Questionnaire, TBQ, 0–150, higher scores indicate higher burden) and HRQoL (Type 1 Diabetes and Life questionnaire for ages 18–25 and 26–45, T1DAL, 0–100, higher scores indicate better HRQoL) among Dutch young adults with T1D (aged 18–30). Results In total, 294 young adults with T1D completed the survey. Mean TBQ score was 59.5 (SD = 24.9). Regular medical care reminding participants of their health problems scored highest. Mean T1DAL scores were 55.9 (SD = 12.9) for ages 18–25, and 62.1 (SD = 13.2) for ages 26–30. Lowest scores were in the subcategory ‘Emotional experiences and daily activities’ (18–25: median = 41.7, IQR = 24.9; 26–30: median = 47.8, IQR = 22.5). TBQ was strongly negatively correlated with T1DAL ( r = −0.69, 95% CI [−0.74, −0.62], p < 0.001). Characteristics associated with higher treatment burden and lower HRQoL included female gender, lower time in range and dissatisfaction with diabetes management approach. Conclusion Young adults with T1D report considerable treatment burden and moderate HRQoL, suggesting a high impact of diabetes care on their lives. Treatment burden is particularly affected by regular medical care activities, whereas diabetes affects the daily functioning and emotional experiences domains of HRQoL. Further research is needed to understand how young adults make care fit and to improve care for these patients, resulting in minimally disruptive care plans. While cautiously interpreted, this may be especially relevant for women and those with adverse clinical outcomes.

AbstractYoung adults living with type 1 diabetes often struggle to achieve what clinicians consider to be optimal levels of metabolic control. Despite the impact that this can have on a young person's future risk of complications, there are relatively few studies reporting new ways of organizing or delivering care to this cohort. In this article, we explore some of the reasons why young adult diabetes care is challenging, and describe approaches to “re‐imagining” how care might be improved. The work is informed by the ‘Making Care Fit’ collaborative and by a program of research, entitled D1 Now, involving co‐design of a complex person‐centered intervention with young adults.

NIDDM is associated with excessive rates of endogenous glucose production in both the postabsorptive and postprandial states. To determine whether this is due to an intrinsic increase in hepatic sensitivity to glucagon, 9 NIDDM and 10 nondiabetic subjects were studied on three occasions. On each occasion, glycogen was labeled the evening before the study with subjects ingesting meals containing [6-3H]galactose. Beginning at 6:00 A.M. on the following morning, somatostatin was infused to inhibit endogenous hormone secretion. Insulin concentrations were maintained constant at basal levels (defined as that necessary to keep glucose at ∼5 mmol/l) in each individual. On one occasion, glucagon was infused at a rate of 0.65 ng ∼ kg−1 · min−1 throughout the experiment, resulting in glucagon concentrations of ∼130 pg/ml and a slow but comparable fall in endogenous glucose production with time in both groups. On the other two occasions, the glucagon infusion was increased at 10:00 A.M. to either 1.5 or 3.0 ng · kg−1 · min−1, resulting in an increase in glucagon concentrations to ∼180 and 310 pg/ml, respectively. The increment in endogenous glucose production (i.e., area above basal) did not differ in diabetic and nondiabetic subjects during either the 1.5 ng · kg−1 · min−1 (0.75 ± 0.055 vs. 0.78 ± 0.048 mmol/kg) or 3.0 ng · kg−1 · min−1 (1.06 ± 0.066 vs. 1.10 ± 0.073 mmol/kg) glucagon infusions. In contrast, the amount of [6-3H]glucose released from glycogen was lower (P &lt; 0.05) in the diabetic than nondiabetic subjects during both glucagon infusions. The specific activity of glycogen, calculated as the integrated release of [6-3H]glucose divided by the integrated release of unlabeled glucose, was lower (P &lt; 0.05) in diabetic subjects than in nondiabetic subjects during both the 1.5 ng · kg−1 · min−1 (19.0 ± 3.9 vs. 41.4 ± 5.7 dpmμmol) and 3.0 ng · kg−1 · min−1 (19.1 ± 3.1 vs. 36.5 ± 7.2 dpm/μmol) glucagon infusions, implying that a greater portion of the glucose released from glycogen was derived from the indirect pathway. We concluded that although NIDDM is not associated with an intrinsic alteration in hepatic sensitivity to glucagon, it does alter the relative contributions of the direct and indirect pathways to nocturnal glycogen synthesis.