Partial sleep deprivation during only a single night induces insulin resistance in multiple metabolic pathways in healthy subjects. This physiological observation may be of relevance for variations in glucoregulation in patients with type 1 and type 2 diabetes.

Introduction:The association between type 1 diabetes (T1D) and other auto-immune diseases is well known. However, a quantitative overview of all associated auto-immune diseases and their prevalence in T1D is lacking. Methods: We searched PubMed, Web of Science, EMBASE and Cochrane library in September 2018 to identify relevant articles about the prevalence of the following associated auto-immune diseases in T1D cohorts: auto-immune thyroid disease, celiac disease, gastric autoimmunity including pernicious anemia, vitiligo and adrenal gland insufficiency. A meta-analysis was performed to estimate pooled prevalence using a random-effects model. Furthermore, randomeffects meta-regression analysis was performed to assess the association between prevalence and mean age or diabetes duration. Results: One hundred eighty articles were eligible including a total of 293 889 type 1 diabetes patients. Hypothyroidism (65 studies) was prevalent in 9.8% (95% CI: 7.5-12.3) of patients. Meta-regression showed that for every 10-year age increase, hypothyroidism prevalence increased 4.6% (95% CI: 2.6-6.6, P < 0.000, 54 studies). Weighted prevalence of celiac disease was 4.5% (95% CI: 4.0-5.5, 87 studies). Gastric autoimmunity was found in 4.3% of patients (95% CI: 1.6-8.2, 8 studies) and vitiligo in 2.4% (95% CI: 1.2-3.9, 14 studies) of patients. The prevalence of adrenal insufficiency was 0.2% (95% CI: 0.0-0.4, 14 studies) and hyperthyroidism was found in 1.3 percent (95% CI: 0.9-1.8, 45 studies) of type 1 diabetes patients. For all analyses, statistical heterogeneity between studies was moderate to high. Conclusions: The prevalence of antibody-mediated auto-immune disease is high among type 1 diabetes patients. Especially hypothyroidism and celiac disease are frequently found.

We conclude that prolonged subclinical hyperthyroidism is accompanied by diastolic dysfunction that is at least partly reversible after restoration of euthyroidism. Because isolated diastolic dysfunction may be associated with increased mortality, this finding is of clinical significance.

The majority of Dutch patients with HNPGL present with a positive family history, in contrast to other European countries. The clinical characteristics of patients with HNPGL are chiefly determined by founder mutations in SDHD, the major causative gene in both familial and isolated patients with HNPGL. The high frequency of founder mutations in SDHD suggests a higher absolute prevalence of paraganglioma syndrome in the Netherlands.

OBJECTIVE -Sleep restriction results in decreased insulin sensitivity and glucose tolerance in healthy subjects. We hypothesized that sleep duration is also a determinant of insulin sensitivity in patients with type 1 diabetes.RESEARCH DESIGN AND METHODS -We studied seven patients (three men, four women) with type 1 diabetes: mean age 44 Ϯ 7 years, BMI 23.5 Ϯ 0.9 kg/m 2 , and A1C 7.6 Ϯ 0.3%. They were studied once after a night of normal sleep duration and once after a night of only 4 h of sleep. Sleep characteristics were assessed by polysomnography. Insulin sensitivity was measured by hyperinsulinemic euglycemic clamp studies with an infusion of [6,6-2 H 2 ]glucose.RESULTS -Sleep duration was shorter in the night with sleep restriction than in the unrestricted night (469 Ϯ 8.5 vs. 222 Ϯ 7.1 min, P ϭ 0.02). Sleep restriction did not affect basal levels of glucose, nonesterified fatty acids (NEFAs), or endogenous glucose production. Endogenous glucose production during the hyperinsulinemic clamp was not altered during the night of sleep restriction compared with the night of unrestricted sleep (6.2 Ϯ 0.8 vs. 6.9 Ϯ 0.6 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , NS). In contrast, sleep restriction decreased the glucose disposal rate during the clamp (25.5 Ϯ 2.6 vs. 22.0 Ϯ 2.1 mol ⅐ kg lean body mass Ϫ1 ⅐ min Ϫ1 , P ϭ 0.04), reflecting decreased peripheral insulin sensitivity. Accordingly, sleep restriction decreased the rate of glucose infusion by ϳ21% (P ϭ 0.04). Sleep restriction did not alter plasma NEFA levels during the clamp (143 Ϯ 29 vs. 133 Ϯ 29 mol/l, NS).CONCLUSIONS -Partial sleep deprivation during a single night induces peripheral insulin resistance in these seven patients with type 1 diabetes. Therefore, sleep duration is a determinant of insulin sensitivity in patients with type 1 diabetes.