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1.
BMJ. 2018 Dec 6;363:k5155. doi: 10.1136/bmj.k5155.

Incretins and cancer of the bile duct in type 2 diabetes.

Author information

1
Addenbrooke's Hospital, Cambridge, UK.
PMID:
30522996
DOI:
10.1136/bmj.k5155
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Conflict of interest statement

Competing interests: I have read and understood the BMJ policy on declaration of interests and declare the following: none.

2.
Diabet Med. 2018 Dec 7. doi: 10.1111/dme.13875. [Epub ahead of print]

Dietary protein affects both the dose and pattern of insulin delivery required to achieve postprandial euglycaemia in Type 1 diabetes: a randomized trial.

Evans M1,2, Smart CEM3,4, Paramalingam N1,2,5, Smith G2, Jones TW1,2,5, King BR3,4,6, Davis EA1,2,5.

Author information

1
Princess Margaret Hospital for Children, Perth, WA.
2
Telethon Kids Institute, University of Western Australia, Perth, WA.
3
John Hunter Children's Hospital, Newcastle, NSW.
4
Hunter Medical Research Institute, Newcastle, NSW.
5
University of Western Australia, Perth, WA.
6
University of Newcastle, Newcastle, NSW, Australia.

Abstract

AIM:

To quantify the insulin requirement for a high-protein meal compared with a low-protein meal, controlling for carbohydrate and fat content.

METHODS:

In this crossover study, young people with Type 1 diabetes were randomized to consume a high- (60 g) or low-protein meal (5 g), each containing 30 g carbohydrate and 8 g fat. A variation of the insulin clamp technique was used to determine the insulin requirements to maintain euglycaemia for the following 5 h.

RESULTS:

A total of 11 participants (mean ± sd age 16.5 ± 2.7 years, HbA1c 52 ± 8.7 mmol/mol [6.9 ± 0.8%], diabetes duration 6.9±5.1 years) completed the study. The mean insulin requirements for the high-protein meal were higher than for the low-protein meal [10.3 (CI 8.2, 12.57) vs 6.7 units (CI 4.7, 8.8); P=0.001], with inter-individual requirements ranging from 0.9 to six times the low-protein meal requirement. Approximately half the additional insulin [1.1 units/h (CI 0.5, 1.8; P=0.001)] was given in the first 2 h, compared with an additional 0.5 units/h (CI -0.2, 1.2; P=0.148) in the second 2 h and 0.1 units (CI -0.6, 0.8; P=0.769) in the final hour.

CONCLUSIONS:

A high-protein meal requires ~50% more insulin to maintain euglycaemia than a low-protein meal that contains the same quantity of carbohydrate. The majority is required within the first 2 h. Inter-individual differences exist in insulin requirements for dietary protein. This article is protected by copyright. All rights reserved.

PMID:
30537305
DOI:
10.1111/dme.13875
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3.
Diabet Med. 2018 Dec 7. doi: 10.1111/dme.13876. [Epub ahead of print]

Diabetic retinopathy in people with Type 2 diabetes and obesity treated by Roux-en-Y gastric bypass compared with non-operated controls: with focus on the role of diabetes remission in a cross-sectional and a 6-year follow-up study.

Author information

1
Department of Endocrinology and Internal Medicine, Aarhus University, Aarhus, Denmark.
2
Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark.
3
Department of Ophthalmology, Aarhus University Hospital, Aarhus, Denmark.

Abstract

AIM:

Whether or not Roux-en-Y gastric bypass (RYGB) and the derived metabolic improvements are beneficial to diabetic retinopathy is controversial. We aimed to determine the presence and development of retinopathy in individuals with obesity and Type 2 diabetes treated by RYGB compared with non-operated controls, and to determine the role of diabetes remission.

METHODS:

We graded fundus photography using the Wisconsin Epidemiologic Study of Diabetic Retinopathy in 96 individuals with obesity and Type 2 diabetes treated by RYGB 6 years after surgery compared with 48 non-operated controls. In a subsample, we investigated the development of retinopathy over time. In the secondary analysis, we divided the RYGB group according to diabetes remission.

RESULTS:

RYGB surgery was not statistically associated with less retinopathy [relative risk (RR) 0.82, 95% CI 0.59 to 1.14], when adjusted for diabetes duration, sex, age and BMI. During 5.9 years of follow-up, retinopathy grading in the RYGB group was unchanged, whereas the control group displayed worse grading by 0.69 steps (95% CI 0.18 to 1.19). The RYGB group with diabetes remission (52%) showed a trend towards less retinopathy [adjusted RR (aRR) 0.45; 95% CI 0.19 to 1.06] than controls, and less retinopathy (aRR 0.33; 95% CI 0.11 to 0.94) than the RYGB group without remission in the cross-sectional data.

CONCLUSIONS:

In a cross-sectional setting, individuals with Type 2 diabetes treated by RYGB showed a tendency towards less retinopathy than non-operated controls, in particular diabetes remission following RYGB was associated with less retinopathy. Moreover after 5.9 years, retinopathy in the RYGB group had progressed less than in the control group. (Clinical Trial Registry No: NCT02625649).

PMID:
30537170
DOI:
10.1111/dme.13876
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4.
Diabet Med. 2018 Dec 7. doi: 10.1111/dme.13865. [Epub ahead of print]

Physical exercise and non-insulin glucose-lowering therapies in the management of Type 2 diabetes mellitus: a clinical review.

Author information

1
Diabetes Research Group, Swansea University, Medical School, Swansea, UK.
2
Applied Sport, Technology, Exercise and Medicine Research Centre (A-STEM), College of Engineering, Swansea University, Swansea, UK.
3
Department of Diabetes and Endocrinology, Morriston Hospital, Swansea, UK.

Abstract

In the UK the National Institute of Health and Care Excellence (NICE) advocates intensive lifestyle programmes that attain the levels of daily physical activity set out by the Chief Medical Officer as a first-line strategy for improving the health of people at risk of developing diabetes or reducing the risk of development of Type 2 diabetes. For people with Type 2 diabetes, lifestyle measures complement pharmacological treatments that include both oral and injectable therapies. In line with this, NICE guidelines also support intensification of efforts to improve patient lifestyle along with these glucose-lowering therapies. There is a paucity of evidence, however, in the available published literature examining the association between glucose-lowering therapies and exercise metabolism. In the present review we explore the current knowledge with regard to the potential interactions of oral and non-insulin injectable therapies with physical activity in people at risk of, or who have, Type 2 diabetes, and present evidence that may inform healthcare professionals of the need to monitor patients more closely in their adaptation to both pharmacological therapy and physical activity.

PMID:
30536728
DOI:
10.1111/dme.13865
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Publication type

Publication type

5.
Diabetes. 2018 Dec 6. pii: db180313. doi: 10.2337/db18-0313. [Epub ahead of print]

Identification of Specific MicroRNAs in Neutrophils of type 2 Diabetic Mice: Overexpression of microRNA-129-2-3p Accelerates Diabetic Wound Healing.

Author information

1
Division of Forensic Pathology and Science, Unit of Social Medicine, Course of Medical and Dental Sciences, Graduate School of Biomedical Sciences, Nagasaki University School of Medicine, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan umehara@nagasaki-u.ac.jp.
2
Department of Pathology, Nagasaki University School of Medicine and Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
3
Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom.
4
Division of Forensic Pathology and Science, Unit of Social Medicine, Course of Medical and Dental Sciences, Graduate School of Biomedical Sciences, Nagasaki University School of Medicine, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.

Abstract

Neutrophils are involved in the first stage of acute inflammation. Following injury, they are mobilized and recruited to the injured tissue. In diabetes, wound healing is delayed and aberrant, leading to excessive recruitment and retention of neutrophils that fail to promote angiogenesis and prolong inflammation. However, the exact pathological mechanisms of diabetic-derived neutrophils in chronic inflammation remain unclear. Here, microRNA (miRNA) profiling of neutrophils from bone marrow in type 2 diabetic mice was performed using a microarray. miRNAs regulate the post-transcriptional expression of target mRNAs and are important in countering inflammation-related diseases. Our study revealed that miRNAs exhibited differential expression in diabetic-derived neutrophils compared with non-diabetic-derived neutrophils, especially miR-129 family members. miR-129-2-3p directly regulated the translation of Casp6 and Ccr2, which are involved in inflammatory responses and apoptosis. Furthermore, miR-129-2-3p overexpression at the wound site of type 2 diabetic mice accelerated wound healing. These results suggest possible involvement of miR-129-2-3p in diabetic-derived neutrophil dysfunction and that retention kinetics of neutrophils and chronic inflammation may be initiated via miR-129-2-3p-regulated genes. This study characterized changes in global miRNA expression in diabetic-derived neutrophils and systematically identified critical target genes involved in certain biological processes related to the pathology of diabetic wound healing.

PMID:
30523028
DOI:
10.2337/db18-0313
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6.
Diabetes. 2018 Dec 6. pii: db181077. doi: 10.2337/db18-1077. [Epub ahead of print]

Multimodal Imaging of the Initial Stages of Diabetic Retinopathy. Different Disease Pathways in Different Patients.

Author information

1
AIBILI - Association for Innovation and Biomedical Research on Light and Image, Coimbra, Portugal.
2
University of Coimbra, Coimbra, Portugal.
3
Advanced Development, Carl Zeiss Meditec, Inc., Dublin, CA.
4
AIBILI - Association for Innovation and Biomedical Research on Light and Image, Coimbra, Portugal cunhavaz@aibili.pt.

Abstract

To evaluate the prevalence of different disease pathways (ischemia, neurodegeneration and edema) in the initial stages of diabetic retinopathy (DR).In this retrospective cross-sectional study, eyes were grouped by DR severity using the 7-field ETDRS protocol (levels 10-20, 35 and 43-47). Neurodegeneration was identified by thinning of the retinal nerve fiber layer (RNFL) and/or ganglion cell layer (GCL). Edema was identified by thickening of the inner nuclear layer (INL), outer plexiform layer (OPL), or full retina. Ischemia was identified by metrics of retinal vessel density.142 eyes from 142 patients (28% women) aged 52-88 years were imaged. Vessel density (ischemia) was significantly different between ETDRS groups (p<0.020). On multivariate regression analysis, it remained significantly different between stages of the disease and showed associations with age (p<0.001), gender (p=0.028) and metabolic control (p=0.034). No significant differences between ETDRS groups were found in retinal thinning (neurodegeneration) or retinal thickness (edema). Eyes with the same ETDRS retinopathy grading from different diabetic patients show that the prevalence of different disease pathways, varies between patients even within the same severity group.Ischemia (capillary dropout) is the only disease pathway that shows correlation with retinopathy severity and metabolic control.

PMID:
30523027
DOI:
10.2337/db18-1077
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7.
Diabetes. 2018 Dec 6. pii: db180416. doi: 10.2337/db18-0416. [Epub ahead of print]

FoxO Transcription Factors are Critical Regulators of Diabetes-Related Muscle Atrophy.

Author information

1
Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
2
Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
3
Division of Endocrinology and Metabolism, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA.
4
Bioinformatics Core, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
5
Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA.
6
Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA C.Ronald.Kahn@joslin.harvard.edu.

Abstract

Insulin deficiency and uncontrolled diabetes lead to a catabolic state with decreased muscle strength, contributing to disease-related morbidity. FoxO transcription factors are suppressed by insulin and thus are key mediators of insulin action. To study their role in diabetic muscle wasting, we created mice with muscle-specific triple knockout of FoxO1/3/4 and induced diabetes in these M-FoxO-TKO mice with streptozotocin (STZ). Muscle mass and myofiber area were decreased 20-30% in STZ-Diabetes mice due to increased ubiquitin-proteasome degradation and autophagy alterations, characterized by increased LC3 containing vesicles, and elevated levels of p-ULK1 and LC3-II. Both the muscle loss and markers of increased degradation/autophagy were completely prevented in STZ-FoxO-TKO mice. Transcriptomic analyses revealed FoxO-dependent increases in ubiquitin-mediated proteolysis pathways in STZ-Diabetes, including regulation of Fbxo32 (Atrogin1), Trim63 (MuRF1), Bnip3L, and Gabarapl. These same genes were increased 1.4- to 3.3-fold in muscle from type 1 diabetics after short-term insulin deprivation. Thus, FoxO-regulated genes play a rate-limiting role in increased protein degradation and muscle atrophy in insulin-deficient diabetes.

PMID:
30523026
DOI:
10.2337/db18-0416
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8.
Diabetes. 2018 Dec 6. pii: db180498. doi: 10.2337/db18-0498. [Epub ahead of print]

Peripheral Mechanisms Mediating the Sustained Anti-Diabetic Action of FGF1 in the Brain.

Author information

1
University of Washington Medicine Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, USA.
2
Department of Pediatric Gastroenterology and Hepatology, University of Washington, Seattle, WA, USA.
3
Department of Physiology, Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, USA.
4
Novo Nordisk A/S, Måløv, Denmark.
5
New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
6
Diabetes and Obesity Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
7
Department of Dental Public Health Sciences, School of Dentistry, University of Washington, Seattle, WA, USA.
8
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA.
9
University of Washington Medicine Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, USA mschwart@u.washington.edu.

Abstract

We recently reported that in rodent models of type 2 diabetes (T2D), a single intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1) induces remission of hyperglycemia that is sustained for weeks. To clarify the peripheral mechanisms underlying this effect, we employed the Zucker diabetic fatty fa/fa rat model of T2D, which, like human T2D, is characterized by progressive deterioration of pancreatic β-cell function after hyperglycemia onset. We report that while icv injection of FGF1 delays the onset of β-cell dysfunction in these animals, it has no effect on either glucose-induced insulin secretion or insulin sensitivity. These observations suggest that FGF1 acts in the brain to stimulate insulin-independent glucose clearance. Based on our finding that icv FGF1 treatment increases hepatic glucokinase gene expression, we considered the possibility that increased hepatic glucose uptake (HGU) contributes to the insulin-independent glucose-lowering effect of icv FGF1. Consistent with this possibility, we report that icv FGF1 injection increases liver glucokinase activity by a ∼2-fold. We conclude that sustained remission of hyperglycemia induced by the central action of FGF1 involves both preservation of β-cell function and stimulation of HGU via increased hepatic glucokinase activity.

PMID:
30523024
DOI:
10.2337/db18-0498
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9.
Diabetes Care. 2018 Dec 6. pii: dc180261. doi: 10.2337/dc18-0261. [Epub ahead of print]

Cost-effectiveness Analysis of Routine Screening Using Massively Parallel Sequencing for Maturity-Onset Diabetes of the Young in a Pediatric Diabetes Cohort: Reduced Health System Costs and Improved Patient Quality of Life.

Author information

1
Department of Endocrinology and Diabetes, Lady Cilento Children's Hospital, South Brisbane, Queensland, Australia.
2
Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Translational Research Institute, Woolloongabba, Queensland, Australia.
3
University of Queensland Diamantina Institute, Translational Research Institute, Woolloongabba, Queensland, Australia.
4
Faculty of Medicine, University of Queensland, Herston, Queensland, Australia.
5
Australian Centre for Health Services Innovation, Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Brisbane, Queensland, Australia.
6
School of Pharmacy, University of Queensland, Woolloongabba, Queensland, Australia.
7
Department of Diabetes and Endocrinology, Perth Children's Hospital, Perth, Western Australia, Australia.
8
Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia.
9
School of Paediatrics and Child Health, University of Western Australia, Perth, Western Australia, Australia.
10
Institute of Health and Biomedical Innovation, Faculty of Health, Queensland University of Technology, Translational Research Institute, Woolloongabba, Queensland, Australia emma.duncan@qut.edu.au.
11
Department of Endocrinology, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia.

Abstract

OBJECTIVE:

Maturity-onset diabetes of the young (MODY) is an autosomal dominant form of diabetes, with multiple causative genes. Some MODY subtypes can be treated with sulfonylureas instead of insulin, improving glycemic control, complication rates, quality of life (QoL), and costs. Using massively parallel sequencing (MPS), we recently determined the prevalence of pathogenic/likely pathogenic MODY variants in an Australian pediatric diabetes cohort. Here, these data are used to estimate cost-effectiveness of using MPS for MODY in all pediatric diabetes cases compared with standard practice (sequencing limited to individuals with specific clinical features).

RESEARCH DESIGN AND METHODS:

A Markov decision model was developed to estimate incremental costs and quality-adjusted life-years (QALYs) of MPS screening, modeled over 30 years. We used our observed prevalence of 2.14% compared with 0.7% for standard practice, based on published data. The probabilities and utility weightings of long-term diabetes complications were based on HbA1c and estimated from published data. A series of one-way sensitivity analyses were performed using the net monetary benefit framework.

RESULTS:

Routine MPS screening for MODY was more effective and less costly than standard care screening, with 26 QALYs gained and 1,016,000 AUD (782,000 USD) saved per 1,000 patients. Cost of screening was fully offset within 10 years. Routine MPS screening remained dominant until MODY prevalence fell to <1.1%.

CONCLUSIONS:

Routine MPS screening for MODY in the pediatric population with diabetes could reduce health system costs and improve patient QoL. Our results make a compelling argument for routine genetic screening in all children with presumed type 1 diabetes mellitus.

PMID:
30523035
DOI:
10.2337/dc18-0261
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10.
Diabetes Care. 2018 Dec 6. pii: dc181556. doi: 10.2337/dc18-1556. [Epub ahead of print]

Incidence and Determinants of Intraocular Lens Implantation in Type 2 Diabetes: The Fremantle Diabetes Study Phase II.

Author information

1
Medical School, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia, Australia.
2
Medical School, University of Western Australia, Fremantle Hospital, Fremantle, Western Australia, Australia tim.davis@uwa.edu.au.
3
Lions Eye Institute, Nedlands, Western Australia, Australia.
4
Centre for Ophthalmology and Visual Science, University of Western Australia, Crawley, Western Australia, Australia.

Abstract

OBJECTIVE:

To compare the incidence of intraocular lens (IOL) implantation for cataracts between people with and without type 2 diabetes and to determine associated risk factors in those with type 2 diabetes.

RESEARCH DESIGN AND METHODS:

Participants with type 2 diabetes (n = 1,499) from the community-based observational Fremantle Diabetes Study Phase II (FDS2) were age, sex, and zip code matched 1:4 with residents without diabetes. IOL implantation status was ascertained between entry (2008-2011) and the end of 2016 using validated data linkage. Age-specific incidence rates and incidence rate ratios (IRRs) for cataract surgery were calculated. Predictors of IOL implantation in FDS2 participants were assessed using proportional hazards and competing risk regression modeling.

RESULTS:

The crude IRR (95% CI) for cataract surgery in FDS2 participants (mean ± SD age 62.8 ± 10.8 years at entry) versus the matched group without diabetes was 1.50 (1.32-1.71), with the highest relative risk in those aged 45-54 years at the time of surgery (7.12 [2.05-27.66]). Competing risk analysis showed that age at entry, diabetes duration, serum HDL cholesterol, serum triglycerides, a severe hypoglycemic episode in the past year, and Asian and southern European ethnicity increased the risk of cataract surgery in participants with type 2 diabetes (P ≤ 0.025).

CONCLUSIONS:

People with type 2 diabetes, especially those in younger age-groups, are at a significantly increased risk of cataract surgery than matched people without diabetes. Multifaceted prevention strategies should be incorporated as part of routine care. As well as limiting ultraviolet light exposure, these might include lipid-modifying treatment and strategies to avoid severe hypoglycemia.

PMID:
30523034
DOI:
10.2337/dc18-1556
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11.
Diabetes Care. 2018 Dec 6. pii: dc181809. doi: 10.2337/dc18-1809. [Epub ahead of print]

Retinopathy and RAAS Activation: Results From the Canadian Study of Longevity in Type 1 Diabetes.

Author information

1
Division of Endocrinology and Metabolism, Sunnybrook Health Sciences Centre, Department of Medicine, University of Toronto, Toronto, Ontario, Canada julie.lovshin@sunnybrook.ca.
2
Division of Nephrology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
3
Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
4
Division of Endocrinology, Department of Pediatrics, and Division of Nephrology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO.
5
Research Division, Joslin Diabetes Center, Boston, MA.
6
Department of Medical Imaging, Schulich School of Medicine & Dentistry, Western University, Ontario, Canada.
7
Department of Medicine, Division of Neurology, University Health Network, University of Toronto, Toronto, Ontario, Canada.
8
Department of Ophthalmology and Vision Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada.
9
Division of Endocrinology and Metabolism, Department of Medicine, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.
10
Department of Physiology, University of Toronto, Toronto, Ontario, Canada.

Abstract

OBJECTIVE:

The importance of renin-angiotensin-aldosterone system (RAAS) activation in retinopathy for long-standing diabetes is not well understood. We determined retinopathy stage and evaluated associations with other vascular complications before and after physiological RAAS activation in adults with long-standing (≥50 years duration) type 1 diabetes.

RESEARCH DESIGN AND METHODS:

Participants underwent retinal examination by digital funduscopic photography and optical coherence tomography and were classified as having nonproliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), or no diabetic retinopathy (NDR) with or without diabetic macular edema (DME). Neuropathy was measured by clinical neuropathy examination scores, electrophysiologically, and by corneal confocal microscopy. Renal function was measured by inulin and para-aminohippurate clearance methods. Arterial stiffness was measured by applanation tonometry. Renal function, blood pressure, and arterial stiffness were measured before and after RAAS activation with angiotensin II (ANGII). Associations were determined using linear regression.

RESULTS:

Twelve (16%) of the 75 participants had NDR, 39 (52%) had NPDR, and 24 (32%) had PDR. A low overall prevalence of DME (4%) was observed. Those with PDR had worse nerve function and reduced corneal nerve density, were more likely to have macrovascular disease, and had increased arterial stiffness in response to ANGII compared with those with NPDR or NDR. Prevalence of kidney disease or renal hemodynamic function did not differ by retinopathy status.

CONCLUSIONS:

PDR was associated with neuropathy severity and cardiovascular and peripheral vascular disease. In those with PDR, RAAS activation may be linked to vascular stiffening, an effect that persists in long-standing type 1 diabetes.

PMID:
30523033
DOI:
10.2337/dc18-1809
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12.
Diabetes Care. 2018 Dec 6. pii: dc181428. doi: 10.2337/dc18-1428. [Epub ahead of print]

Participating in Mental, Social, and Physical Leisure Activities and Having a Rich Social Network Reduce the Incidence of Diabetes-Related Dementia in a Cohort of Swedish Older Adults.

Author information

1
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, and Stockholm University, Stockholm, Sweden anna.marseglia@ki.se xuweili@tmu.edu.cn weili.xu@ki.se.
2
Aging Research Center, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, and Stockholm University, Stockholm, Sweden.
3
Stress Research Institute, Stockholm University, Stockholm, Sweden.
4
Stockholm Gerontology Research Center, Stockholm, Sweden.
5
Department of Epidemiology and Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, China.

Abstract

OBJECTIVE:

The effect of a healthy lifestyle on diabetes-related dementia remains unknown. We examined whether an active lifestyle and rich social network may counteract the increased risk of dementia in people with diabetes.

RESEARCH DESIGN AND METHODS:

Dementia-free older adults from the Swedish National Study on Aging and Care in Kungsholmen (n = 2,650) were followed up for 10 years. Diabetes was ascertained on the basis of medical history, medication use, medical records, or glycated hemoglobin (HbA1c) ≥6.5% and prediabetes as HbA1c between 5.7 and 6.5%. Dementia was diagnosed by specialists following standard criteria. An active lifestyle was defined as a moderate to high (vs. low) level of engagement in leisure activities or a rich social network (having moderate to rich [vs. poor] social connections and support). Hazard ratios (HRs) of dementia risk were derived from Cox regression models.

RESULTS:

There were 246 incident dementia cases during follow-up. Those with diabetes (n = 243), but not those with prediabetes (n = 921), had greater risk of dementia (adjusted HR 2.0 [95% CI 1.4-2.9]) than diabetes-free participants. Participants with diabetes but low level of engagement in leisure activities (HR 4.2 [95% CI 2.2-8.2]) or a poor social network (HR 3.4 [95% CI 1.9-6.1]) had greater dementia risk than diabetes-free participants with moderate to high levels of leisure activity engagement or a moderate to rich social network. In participants with diabetes, an active lifestyle (high level of engagement in leisure activities or a rich social network) was associated with less of a raised risk (HR 1.9 [95% CI 1.1-3.4]).

CONCLUSIONS:

An active and socially integrated lifestyle may significantly counteract the detrimental effect of diabetes on dementia risk.

PMID:
30523030
DOI:
10.2337/dc18-1428
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13.
Diabetes Care. 2018 Dec 10. pii: dc172625. doi: 10.2337/dc17-2625. [Epub ahead of print]

Proinsulin Secretion Is a Persistent Feature of Type 1 Diabetes.

Abstract

OBJECTIVE:

Abnormally elevated proinsulin secretion has been reported in type 2 and early type 1 diabetes when significant C-peptide is present. We questioned whether individuals with longstanding type 1 diabetes and low or absent C-peptide secretory capacity retained the ability to make proinsulin.

RESEARCH DESIGN AND METHODS:

C-peptide and proinsulin were measured in fasting and stimulated sera from 319 subjects with long-standing type 1 diabetes (≥3 years) and 12 control subjects without diabetes. We considered three categories of stimulated C-peptide: 1) C-peptide positive, with high stimulated values ≥0.2 nmol/L; 2) C-peptide positive, with low stimulated values ≥0.017 but <0.2 nmol/L; and 3) C-peptide <0.017 nmol/L. Longitudinal samples were analyzed from C-peptide-positive subjects with diabetes after 1, 2, and 4 years.

RESULTS:

Of individuals with long-standing type 1 diabetes, 95.9% had detectable serum proinsulin (>3.1 pmol/L), while 89.9% of participants with stimulated C-peptide values below the limit of detection (<0.017 nmol/L; n = 99) had measurable proinsulin. Proinsulin levels remained stable over 4 years of follow-up, while C-peptide decreased slowly during longitudinal analysis. Correlations between proinsulin with C-peptide and mixed-meal stimulation of proinsulin were found only in subjects with high stimulated C-peptide values (≥0.2 nmol/L). Specifically, increases in proinsulin with mixed-meal stimulation were present only in the group with high stimulated C-peptide values, with no increases observed among subjects with low or undetectable (<0.017 nmol/L) residual C-peptide.

CONCLUSIONS:

In individuals with long-duration type 1 diabetes, the ability to secrete proinsulin persists, even in those with undetectable serum C-peptide.

PMID:
30530850
DOI:
10.2337/dc17-2625
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14.
Diabetes Care. 2018 Dec 7. pii: dc181893. doi: 10.2337/dc18-1893. [Epub ahead of print]

Assessing the Association Between GLP-1 Receptor Agonist Use and Diabetic Retinopathy Through the FDA Adverse Event Reporting System.

Author information

1
Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC tianwang@unc.edu.
2
Peking University Ninth School of Clinical Medicine (Beijing Shijitan Hospital, Capital Medical University), Beijing, China.
3
Department of Pharmacy Administration and Clinical Pharmacy, School of Pharmaceutical Sciences, Peking University, Beijing, China.
4
Institute for Drug Evaluation, Peking University Health Science Center, Beijing, China.
5
Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC.
6
Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC.
PMID:
30530488
DOI:
10.2337/dc18-1893
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Publication type

Publication type

15.
Lancet. 2018 Dec 1;392(10162):2325. doi: 10.1016/S0140-6736(18)33015-0.

Type 2 diabetes: the urgent need to protect young people.

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