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Mark Gutniak, Valdemar Grill, Arved Roovete, and Suad Efendic

Abstract.

We have investigated the effects of hyperglycemia in Type II diabetic patients on the somatostatin response to oral glucose. In these patients hyperglycemia prevailed (11.8 ± 1.4 mmol/l) and was markedly increased to a maximum of 18.9 ±1.0 mmol/l following the ingestion of 75 g of glucose. The rise in blood glucose following glucose ingestion failed to induce a rise in plasma levels of somatostatin-like immunoreactivity. Biostator-regulated insulin infusion normalized fasting levels of blood glucose and reduced the hyperglycemia following glucose ingestion, i.e. blood glucose now rose from 4.6 ± 0.1 to a maximum of 7.3 ±0.8 mmol/l. This moderate rise in blood glucose was accompanied by a significant (p <0.05) rise in somatostatin-like immunoreactivity. Somatostatin-28 and somatostatin-14 were separated using a Sephadex G-50 fine column. Biostator treatment suppressed plasma levels of both peptides during fasting conditions. Treatment was also accompanied by a rise in both peptides during the first hour following glucose ingestion; this rise did not occur in the untreated state. In conclusion: lack of somatostatin response to glucose in non-insulin-dependent diabetes mellitus is associated with deranged metabolic control. Unresponsiveness to glucose entails the secretion of both somatostatin-28 and -14.

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Michael Alvarsson, Valdemar E Grill, Alexandre Wajngot, Erol Cerasi, and Suad Efendic

We investigated the stability of the insulin response to glucose in healthy subjects by making retrospective comparisons of insulin responses after two 60 min glucose infusion tests performed many years apart. The subjects (N =49) were divided into two lower and two higher quartiles as assessed by the incremental 0–10 min insulin area during the initial glucose infusion test. Ages were initially 32.3±2.8 years in lower quartiles and 26.6±1.1 in higher quartiles and body mass indexes 21.6±0.6 kg/m2 and 21.8±0.5, respectively. The interval between the first and second glucose infusion tests was 8.1±2.8 years for lower quartiles and 10.4±1.3 for higher quartiles. In lower quartiles, the 0–10 min insulin area at first testing was 157.1±15.9 mU/l × 10 min and at follow-up 202.2±26.6 (+ 29%, NS). In higher quartiles, the insulin area decreased from 654.8±70.6 mU/l × 10 min at first testing to 489.8±53.6 at follow-up (−25%, p<0.05). The 0–60 min glucose area did not change significantly between glucose infusion tests in lower quartiles (+ 5%), but did increase by 12% (p<0.005) in higher quartiles. Only one subject of the lowest quartile at first testing changed to higher quartiles at follow-up. Predictable "regression toward the mean" at follow-up was moderate, hence the individual insulin response to glucose was relatively stable with time. This finding is compatible with the hypothesis that genetic factors are of major importance for the insulin response to glucose.

Open access

Bahareh Rasouli, Tomas Andersson, Per-Ola Carlsson, Mozhgan Dorkhan, Valdemar Grill, Leif Groop, Mats Martinell, Tiinamaja Tuomi, and Sofia Carlsson

Objective

Moderate alcohol consumption is associated with a reduced risk of type 2 diabetes. Our aim was to investigate whether alcohol consumption is associated with the risk of latent autoimmune diabetes in adults (LADA), an autoimmune form of diabetes with features of type 2 diabetes.

Design

A population-based case–control study was carried out to investigate the association of alcohol consumption and the risk of LADA.

Methods

We used data from the ESTRID case–control study carried out between 2010 and 2013, including 250 incident cases of LADA (glutamic acid decarboxylase antibodies (GADAs) positive) and 764 cases of type 2 diabetes (GADA negative), and 1012 randomly selected controls aged ≥35. Logistic regression was used to estimate the odds ratios (ORs) of diabetes in relation to alcohol intake, adjusted for age, sex, BMI, family history of diabetes, smoking, and education.

Results

Alcohol consumption was inversely associated with the risk of type 2 diabetes (OR 0.95, 95% CI 0.92–0.99 for every 5-g increment in daily intake). Similar results were observed for LADA, but stratification by median GADA levels revealed that the results only pertained to LADA with low GADA levels (OR 0.85, 95% CI 0.76–0.94/5 g alcohol per day), whereas no association was observed with LADA having high GADA levels (OR 1.00, 95% CI 0.94–1.06/5 g per day). Every 5-g increment of daily alcohol intake was associated with a 10% increase in GADA levels (P=0.0312), and a 10% reduction in homeostasis model assessment of insulin resistance (P=0.0418).

Conclusions

Our findings indicate that alcohol intake may reduce the risk of type 2 diabetes and type 2-like LADA, but has no beneficial effects on diabetes-related autoimmunity.

Open access

Elin Pettersen Sørgjerd, Robin Mjelle, Vidar Beisvåg, Arnar Flatberg, Valdemar Grill, and Bjørn O Åsvold

Objective

Diabetes is a heterogeneous disease and a precise diagnosis of diabetes subgroups is necessary to initiate proper early treatment and clinical management of the disease. Circulating small RNAs (sRNAs) are potentially diagnostic biomarkers in diseases, including diabetes. Here we aimed to examine whether profiles of circulating sRNAs differed between patients with autoimmune and non-autoimmune diabetes and non-diabetic controls.

Design

This cross-sectional case–control study included participants from the third survey of the HUNT study.

Methods

We performed sRNA sequencing in serum from adult-onset type 1 diabetes (n = 51), type 2 diabetes (n = 50) and latent autoimmune diabetes in adult (LADA, n  = 51), as well as non-diabetic HUNT3 participants as control group (n = 51). Differential expression analysis of the sRNAs was performed in R using limma-voom.

Results

We identified differences in sRNA expression between autoimmune (type 1 diabetes and LADA) and non-autoimmune diabetes (type 2 diabetes) and between patients with diabetes and non-diabetic controls. Focusing on miRNA, we identified 10 differentially expressed mature miRNAs and 30 differentially expressed miRNA variants (isomiRs). We also identified significant changes within other sRNA classes, including a pronounced downregulation of a tRNA fragment in patients with diabetes compared to non-diabetic controls. We created cross-validated sRNA signatures based on the significant sRNAs that distinguished patients with diabetes from non-diabetic controls, and autoimmune from non-autoimmune diabetes, with high specificity and sensitivity. sRNA profiles did not distinguish between type 1 diabetes and LADA.

Conclusions

Circulating sRNAs are differentially expressed between patients with diabetes and non-diabetic controls and between autoimmune and non-autoimmune diabetes.