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1.

Error occurred: The following PMID is not available: 28935719

PMID:
28935719
2.
Diabet Med. 2018 Jan;35(1):12-32. doi: 10.1111/dme.13519. Epub 2017 Nov 3.

Inequalities in glycaemic control, hypoglycaemia and diabetic ketoacidosis according to socio-economic status and area-level deprivation in Type 1 diabetes mellitus: a systematic review.

Author information

1
Institute for Biometrics and Epidemiology, German Diabetes Centre, Leibniz Centre for Diabetes Research at Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
2
German Centre for Diabetes Research (DZD), München-Neuherberg, Germany.

Abstract

AIM:

The aim of this systematic review was to examine the associations of individual-level as well as area-level socio-economic status and area-level deprivation with glycaemic control, hypoglycaemia and diabetic ketoacidosis in people with Type 1 diabetes mellitus.

METHODS:

Ovid MEDLINE was searched to identify relevant cohort, case-control or cross-sectional studies published between January 2000 and June 2015. Search results were screened by title, abstract and keywords to identify eligible publications. Decisions on inclusion or exclusion of full texts were made independently by two reviewers. The Newcastle-Ottawa Scale was used to estimate the methodological quality of included studies. Quality assessment and extracted data of included studies were synthesized narratively and reported according to the PRISMA statement.

RESULTS:

Literature search in Ovid MEDLINE identified 1345 eligible studies. Twenty studies matched our inclusion and exclusion criteria. Two articles were additionally identified through hand search. According to the Newcastle-Ottawa Scale, most of the studies were of average quality. Results on associations of socio-economic status and area-level deprivation with glycaemic control and hypoglycaemia were contradictory between studies. By contrast, lower socio-economic status and higher area-level deprivation were associated with a higher risk for diabetic ketoacidosis in all except one study.

CONCLUSIONS:

Lower socio-economic status and higher area-level deprivation are associated with a higher risk of experiencing diabetic ketoacidosis in people with Type 1 diabetes mellitus. Access to care for socially deprived people needs to be expanded to overcome impairing effects on the course of the condition and to reduce healthcare disparities.

PMID:
28945942
DOI:
10.1111/dme.13519
[Indexed for MEDLINE]
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3.
Diabet Med. 2017 Dec;34(12):1728-1736. doi: 10.1111/dme.13518. Epub 2017 Oct 14.

Premixed vs basal-bolus insulin regimen in Type 2 diabetes: comparison of clinical outcomes from randomized controlled trials and real-world data.

Author information

1
Division of Medical Sciences and Graduate Entry Medicine, School of Medicine, University of Nottingham, Nottingham, UK.

Abstract

AIM:

To evaluate the concordance between data derived from randomized controlled trial (RCT) and real-world estimates of HbA1c and weight change after 24 weeks of initiation of a basal-bolus compared with a premixed insulin regimen in people with Type 2 diabetes.

METHODS:

Data eight RCTs were pooled after a systematic review of studies examining basal-bolus (n = 1893) or premixed (n = 1517) regimens. Real-world data were extracted from the UK primary care dataset for people on basal-bolus (n = 7483) or premixed insulin regimens (n=10 744). The mean differences between HbA1c and weight from baseline were calculated using t-tests, while analysis of variance was used to compare the two treatment regimens. Linear regression analyses were used to determine the predictors of this change.

RESULTS:

Both insulin regimens were associated with HbA1c reductions (real-world data -0.28%; RCT data, -1.4%) and weight gain (real-world data, +0.27 kg; RCT data, +2.96 kg) but there were no significant differences between basal-bolus and premixed insulin. Discordances in the pattern of treatment response were observed, however, between real-world and RCT data for both insulin regimens. For any given baseline HbA1c concentration, the change in HbA1c in the RCTs was greater than in real-world conditions and for those with baseline weight above ~60 kg, RCT data showed overall weight gain in contrast to slight weight loss in the real-world population. Lastly, for both randomized controlled trial and real-world populations, while greater baseline weight was associated with reduced response to treatment, the association was much steeper in the RCT than in the real-world population. In addition, greater baseline weight was associated with greater weight reductions in both premixed insulin and basal-bolus insulin regimens, although to a lesser extent with the latter.

CONCLUSION:

These results highlight specific discrepancies in the HbA1c reduction and weight change in insulin regimen between real world versus RCT populations; with greater reduction in HbA1c and greater increase in weight observed in the RCT population than in the real-world population. Also, the basal-bolus regimens in both real-world and RCT populations showed greater reduction in HbA1c compared to the premix regimen (though more marked in RCTs), while the premix regimen showed greater increase in weight in real-world, as against basal-bolus in the RCT population.

PMID:
28945928
DOI:
10.1111/dme.13518
[Indexed for MEDLINE]
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4.
Diabet Med. 2017 Dec;34(12):1676-1683. doi: 10.1111/dme.13517. Epub 2017 Oct 17.

Attenuated heart rate recovery predicts risk of incident diabetes: insights from a meta-analysis.

Author information

1
Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, School of Medicine, Southeast University, Nanjing, P. R. China.
2
Division of Sports and Rehabilitation Medicine, Ulm University Medical Centre, Ulm, Germany.

Abstract

AIMS:

To assess the association between attenuated heart rate recovery, a non-invasive measure of autonomic dysfunction, and risk of diabetes in the general population.

METHODS:

Databases were searched for cohort studies up to May 2017 that reported the association of heart rate recovery with the risk of diabetes. The overall hazard ratios for slowest vs fastest heart rate recovery (the referent) and for every 10-beats-per-min decrement in heart rate recovery were calculated using a random effects meta-analysis model.

RESULTS:

Four cohort studies with 430 incident cases of diabetes among a total of 9113 participants during a mean follow-up period of 8.1 years were included. Results showed that the slowest heart rate recovery was associated with a higher risk of diabetes (hazard ratio 1.66, 95% CI 1.16 to 2.38) vs the fastest heart rate recovery, and the hazard ratio of risk of diabetes for every 10-beats-per-min decrement in heart rate recovery was 1.29 (95% CI 1.13 to 1.48). No significant interaction effect was observed regarding the efficacy of 1-min and 2-min heart rate recovery in predicting risk of diabetes (both Pfor interaction >0.60); however, a linear dose-response relationship existed for overall studies and for studies using 1-min heart rate recovery as the exposure (both P >0.60 for non-linearity).

CONCLUSIONS:

Attenuated heart rate recovery is associated with an increased risk of diabetes in a dose-dependent manner, and measurement of heart rate recovery is worth recommending as part of diabetes risk assessment in clinical routines.

PMID:
28945922
DOI:
10.1111/dme.13517
[Indexed for MEDLINE]
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5.
Diabet Med. 2017 Dec;34(12):1701-1709. doi: 10.1111/dme.13516. Epub 2017 Oct 14.

High risk of conversion to diabetes in first-degree relatives of individuals with young-onset type 2 diabetes: a 12-year follow-up analysis.

Author information

1
Department of Medicine and Therapeutics, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.
2
Hong Kong Institute of Diabetes and Obesity, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.
3
Li Ka Shing Institute of Health and Sciences, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.
4
Department of Chemical Pathology, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.
5
Department of Haematology, Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong.

Abstract

AIM:

Family history of diabetes is an established risk factor for Type 2 diabetes, but the impact of a family history of young-onset diabetes (onset < 40 years) on future risk of diabetes among first-degree relatives is unclear. In this prospective study, we examined the influence of family history of late- versus young-onset diabetes on the development of diabetes in a young to middle-aged Chinese population.

METHODS:

Some 365 siblings identified through probands with Type 2 diabetes and 452 participants from a community-based health awareness project (aged 18-55 years) who underwent metabolic assessment during the period 1998-2002 were followed to 2012-2013 to determine their glycaemic status. Multivariate logistic regression was performed to investigate the association of family history of diabetes presented at different age categories with development of diabetes.

RESULTS:

In this cohort, 53.4% (n = 167) of participants with a family history of young-onset diabetes, 30.1% (n = 68) of those with a family history of late-onset diabetes and 14.4% (n = 40) of those without a family history developed diabetes. Using logistic regression, family history of diabetes presented at ages ≥ 50, 40-49, 30-39 and < 30 years, increased conversion to diabetes with respective odds ratios of 2.4, 5.8, 9.4 and 7.0 (P < 0.001 for all), after adjustment for socio-economic status, smoking, obesity, hypertension and dyslipidaemia. Among participants without diabetes at baseline, risk association of family history of late-onset diabetes with incident diabetes was not sustained, whereas that of family history of young-onset diabetes remained robust on further adjustment for baseline glycaemic measurements.

CONCLUSIONS:

First-degree relatives of people with Type 2 diabetes, especially relatives of those with young-onset diabetes, are at high risk for diabetes.

PMID:
28945282
DOI:
10.1111/dme.13516
[Indexed for MEDLINE]
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6.
Diabetes. 2017 Dec;66(12):3130-3141. doi: 10.2337/db17-0398. Epub 2017 Sep 26.

Genetically Determined Plasma Lipid Levels and Risk of Diabetic Retinopathy: A Mendelian Randomization Study.

Author information

1
Department of Ophthalmology, Harvard Medical School, Massachusetts Eye and Ear, Boston, MA.
2
Duke-NUS Medical School, National University of Singapore, Singapore.
3
Singapore Eye Research Institute, Singapore National Eye Centre, Singapore.
4
Department of Ophthalmology, Flinders University, Adelaide, South Australia, Australia.
5
Human Genetics Center, The University of Texas Health Science Center at Houston, Houston, TX.
6
Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan.
7
Center for Personalized Medicine, China Medical University Hospital, Taichung, Taiwan.
8
School of Chinese Medicine, China Medical University, Taichung, Taiwan.
9
Genetic Center, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan.
10
Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan.
11
Department of Internal Medicine, Tri-Service General Hospital, Taipei City, Taiwan.
12
Institute for Translational Genomics and Population Sciences, LA BioMed, and Department of Pediatrics, Harbor-UCLA Medical Center, Torrance, CA.
13
Department of Medicine, LA BioMed, Harbor-UCLA Medical Center, Torrance, CA.
14
Department of Statistical Genetics, Harvard T.H. Chan School of Public Health, Boston, MA.
15
Department of Ophthalmology, The University of Mississippi Medical Center, Jackson, MS.
16
Department of Medicine, The University of Mississippi Medical Center, Jackson, MS.
17
Centre for Vision Research, The Westmead Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia.
18
Faculty of Medicine, University of Iceland, Reykjavík, Iceland.
19
Icelandic Heart Association, Kópavogur, Iceland.
20
Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI.
21
Clinical and Medical Affairs, CardioDx, Inc., Redwood City, CA.
22
Cardiovascular Health Research Unit, Division of General Internal Medicine, University of Washington, Seattle, WA.
23
Kaiser Permanente Washington Health Research Institute, Seattle, WA.
24
Division of Epidemiology and Clinical Applications, National Eye Institute, National Institutes of Health, Bethesda, MD.
25
Departments of Medical Genetics, Pediatrics, and Medical Research, China Medical University Hospital, Tiachung, Tiawan.
26
Menzies Institute for Medical Research, University of Tasmania, Hobart, Tasmania, Australia.
27
Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
28
Duke-NUS Medical School, National University of Singapore, Singapore chingyu.cheng@duke-nus.edu.sg.

Abstract

Results from observational studies examining dyslipidemia as a risk factor for diabetic retinopathy (DR) have been inconsistent. We evaluated the causal relationship between plasma lipids and DR using a Mendelian randomization approach. We pooled genome-wide association studies summary statistics from 18 studies for two DR phenotypes: any DR (N = 2,969 case and 4,096 control subjects) and severe DR (N = 1,277 case and 3,980 control subjects). Previously identified lipid-associated single nucleotide polymorphisms served as instrumental variables. Meta-analysis to combine the Mendelian randomization estimates from different cohorts was conducted. There was no statistically significant change in odds ratios of having any DR or severe DR for any of the lipid fractions in the primary analysis that used single nucleotide polymorphisms that did not have a pleiotropic effect on another lipid fraction. Similarly, there was no significant association in the Caucasian and Chinese subgroup analyses. This study did not show evidence of a causal role of the four lipid fractions on DR. However, the study had limited power to detect odds ratios less than 1.23 per SD in genetically induced increase in plasma lipid levels, thus we cannot exclude that causal relationships with more modest effect sizes exist.

PMID:
28951389
PMCID:
PMC5697951
[Available on 2018-12-01]
DOI:
10.2337/db17-0398
[Indexed for MEDLINE]
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MeSH terms

Substance

Grant support

7.
Diabetes. 2017 Dec;66(12):3098-3104. doi: 10.2337/db17-0382. Epub 2017 Sep 26.

Retinal Microperimetry: A New Tool for Identifying Patients With Type 2 Diabetes at Risk for Developing Alzheimer Disease.

Author information

1
Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona (VHIR-UAB), Barcelona, Spain.
2
CIBERDEM, Instituto de Salud Carlos III, Madrid, Spain.
3
Department of Ophthalmology, Hospital San Rafael, Barcelona, Spain.
4
Fundació ACE, Barcelona Alzheimer Treatment & Research Center, Barcelona, Spain.
5
Institut de Recerca Vall d'Hebron, Universitat Autònoma de Barcelona (VHIR-UAB), Barcelona, Spain rafael.simo@vhir.org.

Abstract

Type 2 diabetes is associated with a high risk of cognitive impairment and dementia. Therefore, strategies are needed to identify patients who are at risk for dementia. Given that the retina is a brain-derived tissue, it may provide a noninvasive way to examine brain pathology. The aims of this study were to evaluate whether retinal sensitivity 1) correlates with the specific parameters of brain imaging related to cognitive impairment and 2) discriminates patients with diabetes with mild cognitive impairment (MCI) from those with normal cognition and those with Alzheimer disease (AD). For this purpose, a prospective, nested case-control study was performed and included 35 patients with type 2 diabetes without cognitive impairment, 35 with MCI, and 35 with AD. Retinal sensitivity was assessed by Macular Integrity Assessment microperimetry, and a neuropsychological evaluation was performed. Brain neurodegeneration was assessed by MRI and fludeoxyglucose-18 positron emission tomography (18FDG-PET). A significant correlation was found between retinal sensitivity and the MRI and 18FDG-PET parameters related to brain neurodegeneration. Retinal sensitivity was related to cognitive status (normocognitive > MCI > AD; P < 0.0001). Our results suggest that retinal sensitivity assessed by microperimetry is related to brain neurodegeneration and could be a useful biomarker for identifying patients with type 2 diabetes who are at risk for developing AD.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT02360527.

PMID:
28951388
DOI:
10.2337/db17-0382
[Indexed for MEDLINE]
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8.
Diabetes. 2017 Dec;66(12):3105-3110. doi: 10.2337/db17-0794. Epub 2017 Sep 21.

Effect of Exercise-Induced Lactate Elevation on Brain Lactate Levels During Hypoglycemia in Patients With Type 1 Diabetes and Impaired Awareness of Hypoglycemia.

Author information

1
Department of Radiology and Nuclear Medicine, Radboud University Medical Center, Nijmegen, the Netherlands.
2
Department of Internal Medicine, Radboud University Medical Center, Nijmegen, the Netherlands hanne.rooijackers@radboudumc.nl.
3
Department of Internal Medicine, Radboud University Medical Center, Nijmegen, the Netherlands.
4
Department for Health Evidence, Radboud University Medical Center, Nijmegen, the Netherlands.
5
Department of Pediatrics, Radboud University Medical Center, Nijmegen, the Netherlands.

Abstract

Since altered brain lactate handling has been implicated in the development of impaired awareness of hypoglycemia (IAH) in type 1 diabetes, the capacity to transport lactate into the brain during hypoglycemia may be relevant in its pathogenesis. High-intensity interval training (HIIT) increases plasma lactate levels. We compared the effect of HIIT-induced hyperlacticacidemia on brain lactate during hypoglycemia between 1) patients with type 1 diabetes and IAH, 2) patients with type 1 diabetes and normal awareness of hypoglycemia, and 3) healthy participants without diabetes (n = 6 per group). All participants underwent a hypoglycemic (2.8 mmol/L) clamp after performing a bout of HIIT on a cycle ergometer. Before HIIT (baseline) and during hypoglycemia, brain lactate levels were determined continuously with J-difference-editing 1H-MRS, and time curves were analyzed using nonlinear mixed-effects modeling. At the beginning of hypoglycemia (after HIIT), brain lactate levels were elevated in all groups but most pronounced in patients with IAH. During hypoglycemia, brain lactate decreased ∼30% below baseline in patients with IAH but returned to baseline levels and remained there in the other two groups. Our results support the concept of enhanced lactate transport as well as increased lactate oxidation in patients with type 1 diabetes and IAH.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT02308293.

PMID:
28935628
DOI:
10.2337/db17-0794
[Indexed for MEDLINE]
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9.
J Clin Endocrinol Metab. 2017 Sep 1;102(9):3097-3110. doi: 10.1210/jc.2017-01024.

The Effect of Improved Serum 25-Hydroxyvitamin D Status on Glycemic Control in Diabetic Patients: A Meta-Analysis.

Author information

1
Pure North S'Energy Foundation, Calgary, Alberta T2R 0C5, Canada.
2
College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan S7N 5A2, Canada.
3
Key State Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
4
Institute of Genetics and Developmental Biology, International College, University of Chinese Academy of Sciences, Beijing 100101, China.
5
St. Mary's University, Calgary, Alberta T2X 1Z4, Canada.

Abstract

Background:

Type 2 diabetes is a global health concern, with an increased prevalence and high cost of treatment.

Objective:

The aim of this systematic review and meta-analysis was to determine the effect of vitamin D supplementation and improved vitamin D status on glycemia and insulin resistance in type 2 diabetic patients.

Data Source:

We searched PUBMED/Medline, Cumulative Index to Nursing and Allied Health, and Cochrane Library (until January 2017).

Study Selection:

Prospective clinical trials were selected evaluating the impact of vitamin D supplementation on glycosylated hemoglobin (HbA1c), serum fasting plasma glucose (FPG), and homeostatic model assessment of insulin resistance (HOMA-IR) in diabetic patients.

Data Extraction and Synthesis:

We used a random-effects model to synthesize quantitative data, followed by a leave-one-out method for sensitivity analysis. The systematic review registration was CRD42017059555. From a total of 844 entries identified via literature search, 24 controlled trials (1528 individuals diagnosed with type 2 diabetes) were included. The meta-analysis indicated a significant reduction in HbA1c [mean difference: -0.30%; 95% confidence interval (CI): -0.45 to -0.15, P < 0.001], FPG [mean difference: -4.9 mg/dL (-0.27 mmol/L); 95% CI: -8.1 to -1.6 (-0.45 to -0.09 mmol/L), P = 0.003], and HOMA-IR (mean difference: -0.66; 95% CI: -1.06 to -0.26, P = 0.001) following vitamin D supplementation and significant increase in serum 25-hydroxyvitamin D levels [overall increase of 17 ± 2.4 ng/mL (42 ± 6 nmol/L)].

Conclusions:

Vitamin D supplementation, a minimum dose of 100 µg/d (4000 IU/d), may significantly reduce serum FPG, HbA1c, and HOMA-IR index, and helps to control glycemic response and improve insulin sensitivity in type 2 diabetic patients.

PMID:
28957454
DOI:
10.1210/jc.2017-01024
[Indexed for MEDLINE]
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10.
J Clin Endocrinol Metab. 2017 Nov 1;102(11):4109-4116. doi: 10.1210/jc.2017-00913.

Serum Surfactant Protein D as a Biomarker for Measuring Lung Involvement in Obese Patients With Type 2 Diabetes.

Author information

1
Endocrinology and Nutrition Department, Hospital Universitari Arnau de Vilanova, Institut de Recerca Biomèdica de Lleida, Universitat de Lleida, 25198 Lleida, Catalonia, Spain.
2
Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, 28029 Madrid, Spain.
3
Endocrinology and Nutrition Department, Hospital Universitari Vall d'Hebron, Diabetes and Metabolism Research Unit, Vall d'Hebron Institut de Recerca, Universitat Autònoma de Barcelona, 08035 Barcelona, Catalonia, Spain.
4
Pneumology Department, Hospital Universitari Vall d'Hebron, Vall d'Hebron Institut de Recerca, 08035 Barcelona, Catalonia, Spain.
5
Centro de Investigación Biomédica en Red de Enfermedades Respiratorias, Instituto de Salud Carlos III, 28029 Madrid, Spain.
6
Respiratory Department, Hospital Universitari Arnau de Vilanova-Santa María, Institut de Recerca Biomèdica de Lleida, Universitat de Lleida, 25198 Lleida, Catalonia, Spain.

Abstract

Context:

Lung impairment is a new target for late diabetic complications. Biomarkers that could help identify patients requiring functional respiratory tests have not been reported.

Objective:

Our aim was to examine whether serum surfactant protein D (SP-D) and A (SP-A) could be useful biomarkers of lung damage in obese patients with type 2 diabetes (T2D) without known lung disease.

Design and Setting:

A case-control study conducted in an ambulatory obesity unit.

Patients:

Forty-nine obese patients with T2D and 98 subjects without diabetes matched by age, sex, body mass index, and waist circumference were included.

Interventions:

Serum SP-D and SP-A levels were measured using enzyme-linked immunosorbent assay. Forced spirometry and static pulmonary volume were assessed.

Results:

Patients with T2D exhibited higher serum SP-D concentrations than control subjects (P = 0.006). No differences in serum SP-A concentrations were observed. There was an inverse association between forced expiratory volume in 1 second (FEV1) and serum SP-D (r = -0.265; P = 0.029), as well as a significant positive relationship between SP-D concentration and residual volume (r = 0.293; P = 0.043). From receiver operating characteristic analysis, the best SP-D cutoff to identify a FEV1 <80% of predicted was 132.3 ng/mL (area under the curve, 0.725; sensitivity, 77.7%; specificity, 69.4%). Stepwise multivariate regression analysis showed that serum SP-D concentration ≥132.3 ng/mL was independently associated with a FEV1 <80% of predicted (R2 = 0.406). Only the existence of T2D contributed independently to serum SD-P variance among all subjects (R2 = 0.138).

Conclusions:

Serum SP-D concentration can be a useful biomarker for detecting lung impairment in obese patients with T2D.

PMID:
28945872
DOI:
10.1210/jc.2017-00913
[Indexed for MEDLINE]
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11.
J Clin Endocrinol Metab. 2017 Oct 1;102(10):3814-3821. doi: 10.1210/jc.2017-00892.

Serum Insulin Bioassay Reflects Insulin Sensitivity and Requirements in Type 1 Diabetes.

Author information

1
Department of Internal Medicine, Division of Endocrinology, Erasmus MC, 3015 CE Rotterdam, The Netherlands.
2
Minerva Foundation Institute for Medical Research, 00290 Helsinki, Finland.
3
Department of Endocrinology and Nutrition, Hospital del Mar, 08003 Barcelona, Spain.
4
Endocrinology and Nutrition Section, Joan XXIII University Hospital, IISPV Pere Virgili Health Research Institute, Rovira i Virgili University, 43005 Tarragona, Spain.
5
CIBER Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, 28029 Madrid, Spain.
6
Folkhälsan Research Centre, Folkhälsan Institute of Genetics, Biomedicum Helsinki, 00014 Helsinki, Finland.
7
Department of Medicine, University of Helsinki, 00290 Helsinki, Finland.

Abstract

Context:

Insulin resistance could increase insulin requirements in type 1 diabetes (T1D). Current insulin immunoassays do not detect insulin analogs. Kinase insulin receptor (IR) activation (KIRA) bioassays specific for human IR isoforms A (IR-A) and B (IR-B) permit assessment of all circulating insulin bioactivity. We studied whether IR-A and IR-B KIRA assays are related to direct measures of insulin sensitivity or insulin doses in T1D.

Design:

We evaluated 31 adult patients with T1D (age 45.7 ± 1.6 years, body mass index 28.8 ± 0.7 kg/m2). Serum IR-A and IR-B bioactivities were measured by KIRA bioassays. Insulin sensitivity of glucose production (Ra) was measured by the euglycemic hyperinsulinemic clamp technique in which a low insulin dose (0.4 mU/kg/min for 240 minutes) was combined with D-[3-3H] glucose infusion to measure rates of Ra and utilization and insulin action on antilipolysis from suppression of serum free fatty acids.

Results:

Baseline circulating IR-A bioactivity was 53 ± 7 pmol/L, and IR-B bioactivity was 81 ± 11 pmol/L. Compared with baseline, insulin infusion significantly increased IR-A (P < 0.001) and IR-B (P < 0.001) bioactivities. Fasting IR-A and IR-B bioactivities were positively related to endogenous Ra (r = 0.44, P = 0.01 and r = 0.38, P < 0.05). Fasting IR-A (r = 0.43, P = 0.02) and IR-B (r = 0.47, P = 0.01) bioactivities were significantly correlated with insulin requirements and glycosylated hemoglobin (IR-A: r = 0.52, P = 0.002; IR-B: r = 0.48, P = 0.006).

Conclusions:

Circulating IR-A and IR-B bioactivities are associated with insulin resistance, high insulin requirements, and poor glycemic control in T1D. Measurement of IR bioactivity by KIRA assays provides a tool to assess the amount of biologically active insulin in groups of T1D patients treated with insulin analogs.

PMID:
28938465
DOI:
10.1210/jc.2017-00892
[Indexed for MEDLINE]
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12.
J Clin Endocrinol Metab. 2017 Oct 1;102(10):3848-3857. doi: 10.1210/jc.2017-01354.

Development and Risk Factors of Type 2 Diabetes in a Nationwide Population of Women With Polycystic Ovary Syndrome.

Author information

1
OPEN-Odense Patient Data Explorative Network, Institute of Clinical Research, University of Southern Denmark, 5000 Odense C, Denmark.
2
Department of Endocrinology, Odense University Hospital, 5000 Odense C, Denmark.
3
Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, 5000 Odense C, Denmark.
4
Department of Medicine, Holbaek Hospital, 4300 Holbaek, Denmark.

Abstract

Objective:

Polycystic ovary syndrome (PCOS) is associated with insulin resistance and obesity. Prospective population-based data regarding development and possible predictors of type 2 diabetes (T2D) in PCOS are limited.

Design:

National Patient Register-based study.

Methods:

Patients with PCOS [PCOS Denmark and embedded cohort, PCOS Odense University Hospital (OUH)] and a control population with no previous diagnosis of T2D. PCOS OUH (N = 1,162) included premenopausal women with PCOS and standardized clinical and biochemical examination. PCOS Denmark (N = 18,477) included women with PCOS in the Danish National Patient Register. Three age-matched controls were included per patient (N = 54,680).

Main outcome:

T2D events according to diagnosis codes and filled medicine prescriptions.

Results:

The median (quartiles) follow-up was 11.1 (6.9 to 16.0) years. The hazard ratio (HR) with 95% confidence interval (CI) for development of T2D in PCOS Denmark was HR = 4.0 (95% CI, 3.7 to 4.3; P < 0.001), and the total event rate of T2D was 8.0 per 1000 person years in PCOS Denmark vs 2.0 per 1000 person years in controls (P < 0.001). The median age at diagnosis of T2D was 31 (26 to 37) years in PCOS Denmark vs 35 (27 to 44) years in controls (P < 0.001). In multiple regression analyses, body mass index, glycated hemoglobin, fasting blood glucose, 2-hour blood glucose, homeostasis model assessment of insulin resistance, and triglycerides were positively associated with development of T2D, whereas higher number of births was negatively associated with development of T2D.

Conclusion:

The event rate of T2D was higher in PCOS compared with controls, and T2D was diagnosed at a younger age.

PMID:
28938447
DOI:
10.1210/jc.2017-01354
[Indexed for MEDLINE]
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13.
J Clin Endocrinol Metab. 2017 Nov 1;102(11):4153-4162. doi: 10.1210/jc.2017-01091.

Single-Dose Metformin Enhances Bile Acid-Induced Glucagon-Like Peptide-1 Secretion in Patients With Type 2 Diabetes.

Author information

1
Center for Diabetes Research, Gentofte Hospital, University of Copenhagen, 2900 Hellerup, Denmark.
2
Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, 2100 Copenhagen Ø, Denmark.
3
Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen N, Denmark.
4
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen N, Denmark.
5
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen N, Denmark.
6
Steno Diabetes Center Copenhagen, University of Copenhagen, 2820 Gentofte, Denmark.

Abstract

Context:

Despite a position as the first-line pharmacotherapy in type 2 diabetes, the glucose-lowering mechanisms of metformin remain to be fully clarified. Gut-derived modes of action, including suppression of bile acid reabsorption and a resulting increase in glucagon-like peptide-1 (GLP-1) secretion, have been proposed.

Objective:

The aim of this study was to assess the GLP-1 secretory and glucometabolic effects of endogenously released bile, with and without concomitant single-dose administration of metformin in patients with type 2 diabetes.

Design:

Randomized, placebo-controlled, and double-blinded crossover study.

Setting:

This study was conducted at Center for Diabetes Research, Gentofte Hospital, Denmark.

Patients:

Fifteen metformin-treated patients with type 2 diabetes; all participants completed the study.

Interventions:

Four experimental study days in randomized order with administration of either 1500 mg metformin or placebo in combination with intravenous infusion of cholecystokinin (0.4 pmol × kg-1 × min-1) or saline.

Main Outcome Measure:

Plasma GLP-1 excursions as measured by baseline-subtracted area under the curve.

Results:

Single-dose metformin further enhanced bile acid-mediated induction of GLP-1 secretion (P = 0.02), whereas metformin alone did not increase plasma GLP-1 concentrations compared with placebo (P = 0.17). Metformin, both with (P = 0.02) and without (P = 0.02) concomitant cholecystokinin-induced gallbladder emptying, elicited reduced plasma glucose excursions compared with placebo. No GLP-1-mediated induction of insulin secretion or suppression of glucagon was observed.

Conclusions:

Metformin elicited an enhancement of the GLP-1 response to cholecystokinin-induced gallbladder emptying in patients with type 2 diabetes, whereas no derived effects on insulin or glucagon secretion were evident in this acute setting.

TRIAL REGISTRATION:

ClinicalTrials.gov NCT02497313.

PMID:
28938439
DOI:
10.1210/jc.2017-01091
[Indexed for MEDLINE]
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14.
J Clin Endocrinol Metab. 2017 Oct 1;102(10):3621-3634. doi: 10.1210/jc.2017-00042.

Type 2 Diabetes and Osteoporosis: A Guide to Optimal Management.

Author information

1
Division of Endocrinology and Diabetes, Aghia Sophia Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
2
Department of Endocrinology and Diabetes, Chelsea and Westminster Hospital, London SW10 9NH, United Kingdom.
3
Unit of Reproductive Endocrinology, First Department of Obstetrics and Gynecology, Medical School, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
4
Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, 11526 Athens, Greece.

Abstract

Context:

Both type 2 diabetes (T2D) and osteoporosis are affected by aging and quite often coexist. Furthermore, the fracture risk in patients with T2D is increased. The aim of this article is to review updated information on osteoporosis and fracture risk in patients with T2D, to discuss the effects of diabetes treatment on bone metabolism, as well as the effect of antiosteoporotic medications on the incidence and control of T2D, and to provide a personalized guide to the optimal management.

Evidence Acquisition:

A systematic literature search for human studies was conducted in three electronic databases (PubMed, Cochrane, and EMBASE) until March 2017. Regarding recommendations, we adopted the grading system introduced by the American College of Physicians.

Evidence Synthesis:

The results are presented in systematic tables. Healthy diet and physical exercise are very important for the prevention and treatment of both entities. Metformin, sulfonylureas, dipeptidyl peptidase-4 inhibitors, and glucagon-like peptide-1 receptor agonists should be preferred for the treatment of T2D in these patients, whereas strict targets should be avoided for the fear of hypoglycemia, falls, and fractures. Insulin should be used with caution and with careful measures to avoid hypoglycemia. Thiazolidinediones and canagliflozin should be avoided, whereas other sodium-dependent glucose transporter 2 inhibitors are less well-validated options. Insulin therapy is the preferred method for achieving glycemic control in hospitalized patients with T2D and fractures. The treatment and monitoring of osteoporosis should be continued without important amendments because of the presence of T2D.

Conclusions:

Patients with coexisting T2D and osteoporosis should be managed in an optimal way according to scientific evidence.

PMID:
28938433
DOI:
10.1210/jc.2017-00042
[Indexed for MEDLINE]
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15.
J Clin Endocrinol Metab. 2018 Jan 1;103(1):35-45. doi: 10.1210/jc.2017-01159.

Pancreatic Histopathology of Human Monogenic Diabetes Due to Causal Variants in KCNJ11, HNF1A, GATA6, and LMNA.

Author information

1
Section of Adult and Pediatric Endocrinology, Diabetes, and Metabolism, The University of Chicago, Chicago, Illinois.
2
Department of Pediatrics, University of Florida, Gainesville, Florida.
3
Department of Human Genetics, The University of Chicago, Chicago, Illinois.
4
Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, Florida.

Abstract

Context:

Monogenic diabetes is thought to account for 2% of all diabetes cases, but most patients receive misdiagnoses of type 1 or type 2 diabetes. To date, little is known about the histopathological features of pancreata from patients with monogenic diabetes.

Objective:

Retrospective study of the JDRF Network for Pancreatic Organ Donors with Diabetes biorepository to identify possible cases of monogenic diabetes and to compare effects of genetic variants on pancreas histology.

Methods:

We selected cases of diabetes for genetic testing on the basis of criteria that included young age at diagnosis, low body mass index, negative autoantibody status, and/or detectable C-peptide level. Samples underwent next-generation-targeted sequencing of 140 diabetes/diabetes-related genes. Pancreas weight and histopathology were reviewed.

Results:

Forty-one of 140 cases of diabetes met the clinical inclusion criteria, with 38 DNA samples available. Genetic variants of probable clinical significance were found in four cases: one each in KCNJ11, HNF1A, GATA6, and LMNA. The KCNJ11 and HNF1A samples had significantly decreased pancreas weight and insulin mass similar to that of type 1 diabetes but had no insulitis. The GATA6 sample had severe pancreatic atrophy but with abundant β cells and severe amyloidosis similar to type 2 diabetes. The LMNA sample had preserved pancreas weight and insulin mass but abnormal islet architecture and exocrine fatty infiltrates.

Conclusions:

Four cases of diabetes had putative causal variants in monogenic diabetes genes. This study provides further insight into the heterogeneous nature of monogenic diabetes cases that exhibited clinical and pathophysiological features that overlap with type 1/type 2 diabetes.

PMID:
28938416
PMCID:
PMC5761488
[Available on 2019-01-01]
DOI:
10.1210/jc.2017-01159
[Indexed for MEDLINE]
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16.
N Engl J Med. 2017 Sep 21;377(12):1143-1155. doi: 10.1056/NEJMoa1700459.

Weight and Metabolic Outcomes 12 Years after Gastric Bypass.

Author information

1
From Intermountain Live Well Center Salt Lake, Intermountain Healthcare (T.D.A.), the Division of Cardiovascular Genetics, Department of Internal Medicine (T.D.A., L.E.D., M.N.N., J.M.G., S.J.F., P.N.H., S.C.H.), Division of General Surgery, Department of Surgery (A.R.I.), and Division of Cardiovascular Medicine, Department of Internal Medicine (P.N.H.), University of Utah School of Medicine, the Department of Health, Kinesiology and Recreation, College of Health, University of Utah (J.K.), the Utah Foundation for Biomedical Research and Utah Lipid Center (E.A.B.), and Rocky Mountain Associated Physicians (R.M., S.C.S.), Salt Lake City, and the Department of Exercise Sciences, Brigham Young University, Provo (L.E.D.) - all in Utah; the Medical University of South Carolina and the Ralph H. Johnson Veterans Affairs Medical Center, Charleston (S.E.L.); Quality of Life Consulting, and the Department of Community and Family Medicine, Duke University Health System, Durham, NC (R.L.K.); Western Norway University of Applied Sciences, Department of Health Studies, and Førde Hospital Trust, Førde, and the Morbid Obesity Centre, Vestfold Hospital Trust, Tønsberg - all in Norway (R.L.K.); and the Department of Genetic Medicine, Weill Cornell Medicine, Doha, Qatar (S.J.F., S.C.H.).

Abstract

BACKGROUND:

Few long-term or controlled studies of bariatric surgery have been conducted to date. We report the 12-year follow-up results of an observational, prospective study of Roux-en-Y gastric bypass that was conducted in the United States.

METHODS:

A total of 1156 patients with severe obesity comprised three groups: 418 patients who sought and underwent Roux-en-Y gastric bypass (surgery group), 417 patients who sought but did not undergo surgery (primarily for insurance reasons) (nonsurgery group 1), and 321 patients who did not seek surgery (nonsurgery group 2). We performed clinical examinations at baseline and at 2 years, 6 years, and 12 years to ascertain the presence of type 2 diabetes, hypertension, and dyslipidemia.

RESULTS:

The follow-up rate exceeded 90% at 12 years. The adjusted mean change from baseline in body weight in the surgery group was -45.0 kg (95% confidence interval [CI], -47.2 to -42.9; mean percent change, -35.0) at 2 years, -36.3 kg (95% CI, -39.0 to -33.5; mean percent change, -28.0) at 6 years, and -35.0 kg (95% CI, -38.4 to -31.7; mean percent change, -26.9) at 12 years; the mean change at 12 years in nonsurgery group 1 was -2.9 kg (95% CI, -6.9 to 1.0; mean percent change, -2.0), and the mean change at 12 years in nonsurgery group 2 was 0 kg (95% CI, -3.5 to 3.5; mean percent change, -0.9). Among the patients in the surgery group who had type 2 diabetes at baseline, type 2 diabetes remitted in 66 of 88 patients (75%) at 2 years, in 54 of 87 patients (62%) at 6 years, and in 43 of 84 patients (51%) at 12 years. The odds ratio for the incidence of type 2 diabetes at 12 years was 0.08 (95% CI, 0.03 to 0.24) for the surgery group versus nonsurgery group 1 and 0.09 (95% CI, 0.03 to 0.29) for the surgery group versus nonsurgery group 2 (P<0.001 for both comparisons). The surgery group had higher remission rates and lower incidence rates of hypertension and dyslipidemia than did nonsurgery group 1 (P<0.05 for all comparisons).

CONCLUSIONS:

This study showed long-term durability of weight loss and effective remission and prevention of type 2 diabetes, hypertension, and dyslipidemia after Roux-en-Y gastric bypass. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others.).

PMID:
28930514
PMCID:
PMC5737957
DOI:
10.1056/NEJMoa1700459
[Indexed for MEDLINE]
Free PMC Article
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17.
Transplantation. 2018 Jan;102(1):e39-e40. doi: 10.1097/TP.0000000000001964.

Chronic Liraglutide Administration Fails to Suppress Postprandial Glucagon Levels in Type 1 Diabetic Islet Allograft Recipients With Graft Dysfunction.

Author information

1
Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, FL.
2
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Miami Miller School of Medicine, Miami, FL.
3
Department of Internal Medicine, Framingham Union Hospital, Metrowest Medical Center, Boston, MA.
4
Department of Public Health Sciences, University of Miami, Miami FL.
PMID:
28957843
PMCID:
PMC5741482
[Available on 2019-01-01]
DOI:
10.1097/TP.0000000000001964
[Indexed for MEDLINE]
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