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1.
BMJ. 2019 Feb 28;364:l321. doi: 10.1136/bmj.l321.

Diabetes insipidus.

Author information

1
Department of Endocrinology, University Hospitals of Leicester, Leicester, UK.
2
Department of Endocrinology, Croydon University Hospital, London, UK.
3
Department of Endocrinology, Oxford University Hospital NHS Foundation Trust, Oxford, UK.
PMID:
30819684
DOI:
10.1136/bmj.l321
[Indexed for MEDLINE]
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2.
BMJ. 2018 Nov 22;363:k3119. doi: 10.1136/bmj.k3119.

Are you well controlled?

PMID:
30467109
DOI:
10.1136/bmj.k3119
[Indexed for MEDLINE]
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Conflict of interest statement

Competing interests: Competing interests: The author’s competing interests are held by the journal, and are not related to the content of this article.

3.
Diabet Med. 2019 Feb 25. doi: 10.1111/dme.13942. [Epub ahead of print]

Is it possible to constantly and accurately monitor blood sugar levels, in people with Type 1 diabetes, with a discrete device (non-invasive or invasive)?

Author information

1
Division of Diabetes, Endocrinology and Metabolism, Faculty of Medicine, Imperial College, London, UK.

Abstract

Real-time continuous glucose monitors using subcutaneous needle-type sensors continue to develop. The limitations of currently available systems, however, include time lag behind changes in blood glucose, the invasive nature of such systems, and in some cases, their accuracy. Non-invasive techniques have been developed, but, to date, no commercial device has been successful. A key research priority for people with Type 1 diabetes identified by the James Lind Alliance was to identify ways of monitoring blood glucose constantly and accurately using a discrete device, invasive or non-invasive. Integration of such a sensor is important in the development of a closed-loop system and the technology must be rapid, selective and acceptable for continuous use by individuals. The present review provides an update on existing continuous glucose-sensing technologies, and an overview of emergent techniques, including their accuracy and limitations.

PMID:
30803028
DOI:
10.1111/dme.13942
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Publication type

4.
Diabet Med. 2019 Feb 25. doi: 10.1111/dme.13943. [Epub ahead of print]

Ceramides and diabetes mellitus: an update on the potential molecular relationships.

Author information

1
Chronic Kidney Disease Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2
Department of Medical Sciences, AOU Città della Salute e della Scienza di Torino, University of Turin, Torino, Italy.
3
Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milan, Italy.
4
Neurogenic Inflammation Research Center, Mashhad, Iran.
5
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad, Iran.
6
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.

Abstract

Recent evidence suggests that ceramides can play an important pathophysiological role in the development of diabetes. Ceramides are primarily recognized as lipid bilayer building blocks, but recent work has shown that these endogenous molecules are important intracellular signalling mediators and may exert some diabetogenic effects via molecular pathways involved in insulin resistance, β-cell apoptosis and inflammation. In the present review, we consider the available evidence on the possible roles of ceramides in diabetes mellitus and introduce eight different molecular mechanisms mediating the diabetogenic action of ceramides, categorized into those predominantly related to insulin resistance vs those mainly implicated in β-cell dysfunction. Specifically, the mechanistic evidence involves β-cell apoptosis, pancreatic inflammation, mitochondrial stress, endoplasmic reticulum stress, adipokine release, insulin receptor substrate 1 phosphorylation, oxidative stress and insulin synthesis. Collectively, the evidence suggests that therapeutic agents aimed at reducing ceramide synthesis and lowering circulating levels may be beneficial in the prevention and/or treatment of diabetes and its related complications.

PMID:
30803019
DOI:
10.1111/dme.13943
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5.
Diabet Med. 2019 Feb 22. doi: 10.1111/dme.13941. [Epub ahead of print]

Non-insulin treatments for Type 1 diabetes: critical appraisal of the available evidence and insight into future directions.

Author information

1
University of Washington Medical Center/Roosevelt, Seattle, WA, USA.

Abstract

Intensive insulin therapy is the mainstay of treatment for people with Type 1 diabetes, but hypoglycaemia and weight gain are often limiting factors in achieving glycaemic targets and decreasing the risk of diabetes-related complications. The inclusion of pharmacological agents used traditionally in Type 2 diabetes as adjuncts to insulin therapy in Type 1 diabetes has been explored, with the goal of mitigating such drawbacks. Pramlintide and metformin result in modest HbA1c and weight reductions, but their use is limited by poor tolerability and, in the case of pramlintide, by frequency of injections and cost. The addition of glucagon-like peptide-1 receptor agonists to insulin results in improved glycaemic control, reduced insulin doses and weight loss, but this is at the expense of higher rates of hypoglycaemia and hyperglycaemia with ketosis. Sodium-glucose co-transporter-2 and dual sodium-glucose co-transporter-2 and -1 inhibitors also improve glucose control, but with reductions in weight and insulin requirements potentiating the risk of acidosis-related events and hypoglycaemia. The high proportion of people with Type 1 diabetes not achieving glycaemic targets, the negative clinical impact of intensive insulin therapy and the rise in obesity and cardiovascular disease and mortality, underline the need for individualized clinical care. The evaluation of new therapies, effective in Type 2 diabetes, as adjuncts to insulin therapy represents a promising strategy, particularly given the beneficial effects on cardiovascular and renal outcomes in people with Type 2 diabetes with or at high risk of complications that are also observed in patients with Type 1 diabetes. As the population with Type 1 diabetes ages, our mission is to evolve and provide better tools and improved therapies to excel, not only in glycaemic control but also in risk reduction and reduction of complications.

PMID:
30801765
DOI:
10.1111/dme.13941
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8.
Diabetes. 2019 Feb 22. pii: db190025. doi: 10.2337/db19-0025. [Epub ahead of print]

The Hypothalamic Arcuate Nucleus-Median Eminence is a Target for Sustained Diabetes Remission Induced by Fibroblast Growth Factor 1.

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
Diabetes Research, Global Drug Discovery, Novo Nordisk, Maaleov, Denmark.
4
University of Washington Medicine Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA, USA. mschwart@u.washington.edu.

Abstract

In rodent models of type 2 diabetes (T2D), sustained remission of diabetic hyperglycemia can be induced by a single intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1). To identify the brain area(s) responsible for this effect, we first used immunohistochemistry to map the hypothalamic distribution of phosphoERK (pERK1/2), a marker of MAP kinase-ERK signal transduction downstream of FGF receptor activation. Twenty minutes after icv FGF1 injection in adult male Wistar rats, pERK1/2 staining was detected primarily in two hypothalamic areas: the arcuate nucleus and adjacent median eminence (ARC-ME), and the paraventricular nucleus (PVN). To determine whether an action of FGF1 localized to either the ARC-ME or the PVN is capable of mimicking the sustained antidiabetic effect elicited by icv FGF1, we microinjected either saline vehicle or a low dose of FGF1 (0.3 µg/side) bilaterally into either the ARC-ME area or PVN of Zucker Diabetic Fatty (ZDF) rats, a model of T2D, and monitored daily food intake, body weight, and blood glucose levels over a 3-week period. Whereas bilateral intra-arcuate microinjection of saline vehicle was without effect, remission of hyperglycemia lasting >3 wk was observed following bilateral microinjection of FGF1 into the ARC-ME. This antidiabetic effect cannot be attributed to leakage of FGF1 into cerebrospinal fluid and subsequent action on other brain areas, since icv injection of the same total dose was without effect. Combined with our finding that bilateral microinjection of the same dose of FGF1 into the PVN was without effect on glycemia or other parameters, we conclude that the ARC-ME area (but not the PVN) is a target for sustained remission of diabetic hyperglycemia induced by FGF1.

PMID:
30796029
DOI:
10.2337/db19-0025
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11.
Diabetes Care. 2019 Jan;42(1):e13. doi: 10.2337/dci18-0045.

Response to Comment on Cheung and Moses. Gestational Diabetes Mellitus: Is It Time to Reconsider the Diagnostic Criteria? Diabetes Care 2018;41:1337-1338.

Author information

1
Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, New South Wales, Australia wah.cheung@sydney.edu.au.
2
Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia.
3
Diabetes Services, Illawarra Shoalhaven Local Health District, Wollongong, New South Wales, Australia.
PMID:
30811340
DOI:
10.2337/dci18-0045
[Indexed for MEDLINE]
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13.
Diabetes Care. 2019 Jan;42(1):e10. doi: 10.2337/dci18-0038.

Response to Comment on Li et al. Visual Inspection of Chromatograms Assists Interpretation of HbA1c: A Case Report. Diabetes Care 2018;41:1829-1830.

Li Q1,2, Xiao Y3, Shah AD2,4, Li S5,6.

Author information

1
Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China.
2
Institute of Health Informatics, University College London, London, U.K.
3
Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, China.
4
University College London Hospitals NHS Foundation Trust, London, U.K.
5
Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China lisheyu@gmail.com.
6
Division of Population Health and Genomics, Ninewells Hospital and Medical School, University of Dundee, Dundee, U.K.
14.
Diabetes Care. 2019 Jan;42(1):e9. doi: 10.2337/dc18-1836.

Comment on Li et al. Visual Inspection of Chromatograms Assists Interpretation of HbA1c: A Case Report. Diabetes Care 2018;41:1829-1830.

Author information

1
Department of Laboratory Medicine, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China.
2
Department of Laboratory Medicine, Maternity and Child Healthcare Hospital of Nanshan District, Shenzhen, Guangdong, China.
3
Department of Laboratory Medicine, Peking University Shenzhen Hospital, Shenzhen, Guangdong, China 1120303921@qq.com.
PMID:
30811337
DOI:
10.2337/dc18-1836
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16.
Diabetes Care. 2019 Jan;42(1):e1-e3. doi: 10.2337/DC18-0914.

HbA1c, Insulin Resistance, and β-Cell Function in Relation to Cognitive Function in Type 2 Diabetes: The CAROLINA Cognition Substudy.

Author information

1
Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands j.janssen-9@umcutrecht.nl.
2
Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands.
3
Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands.
4
Department of Neurology, Erasmus MC University Medical Center, Rotterdam, the Netherlands.
5
Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, and Division of Endocrinology, University of Toronto, Toronto, Canada.
6
Department of Biostatistics and Data Science, Wake Forest School of Medicine, Winston-Salem, NC.
7
Department of Internal Medicine and Cardiovascular Research Institute, Maastricht University Medical Center+, Maastricht, the Netherlands.
8
Global Biometrics and Data Management, Boehringer Ingelheim, Ingelheim, Germany.
9
Clinical Development, Therapeutic Area CardioMetabolic, Boehringer Ingelheim, Asker, Norway.
PMID:
30811335
DOI:
10.2337/DC18-0914
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17.
Diabetes Care. 2019 Jan;42(1):1-2. doi: 10.2337/dc19-ti01.

In This Issue of Diabetes Care.

[No authors listed]
PMID:
30811333
DOI:
10.2337/dc19-ti01
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18.
Diabetes Care. 2019 Feb 22. pii: dc182204. doi: 10.2337/dc18-2204. [Epub ahead of print]

Improved Open-Loop Glucose Control With Basal Insulin Reduction 90 Minutes Before Aerobic Exercise in Patients With Type 1 Diabetes on Continuous Subcutaneous Insulin Infusion.

Author information

1
Faculty of Health, School of Kinesiology and Health Science, Muscle Health Research Centre, York University, Toronto, Ontario, Canada.
2
Insulet Canada Corporation, Oakville, Ontario, Canada.
3
Insulet Corporation, Billerica, MA.
4
Faculty of Health, School of Kinesiology and Health Science, Muscle Health Research Centre, York University, Toronto, Ontario, Canada mriddell@yorku.ca.
5
LMC Diabetes & Endocrinology, Toronto, Ontario, Canada.

Abstract

OBJECTIVE:

To reduce exercise-associated hypoglycemia, individuals with type 1 diabetes on continuous subcutaneous insulin infusion typically perform basal rate reductions (BRRs) and/or carbohydrate feeding, although the timing and amount of BRRs necessary to prevent hypoglycemia are unclear. The goal of this study was to determine if BRRs set 90 min pre-exercise better attenuate hypoglycemia versus pump suspension (PS) at exercise onset.

RESEARCH DESIGN AND METHODS:

Seventeen individuals completed three 60-min treadmill exercise (∼50% of VO2peak) visits in a randomized crossover design. The insulin strategies included: 1) PS at exercise onset; 2) 80% BRR set 90 min pre-exercise; and 3) 50% BRR set 90 min pre-exercise.

RESULTS:

Blood glucose level at exercise onset was higher with 50% BRR (191 ± 49 mg/dL) vs. 80% BRR (164 ± 41 mg/dL; P < 0.001) and PS (164 ± 45 mg/dL; P < 0.001). By exercise end, 80% BRR showed the smallest drop (-31 ± 58 mg/dL) vs. 50% BRR (-47 ± 50 mg/dL; P = 0.04) and PS (-67 ± 41 mg/dL; P < 0.001). With PS, 7 out of 17 participants developed hypoglycemia versus 1 out of 17 in both BRR conditions (P < 0.05). Following a standardized meal postexercise, glucose rose with PS and 50% BRR (both P < 0.05), but failed to rise with 80% BRR (P = 0.16). Based on interstitial glucose, overnight mean percent time in range was 83%, 83%, and 78%, and time in hypoglycemia was 2%, 1%, and 5% with 80% BRR, 50% BRR, and PS, respectively (all P > 0.05).

CONCLUSIONS:

Overall, a 50-80% BRR set 90 min pre-exercise improves glucose control and decreases hypoglycemia risk during exercise better than PS at exercise onset, while not compromising the postexercise meal glucose control.

PMID:
30796112
DOI:
10.2337/dc18-2204
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19.
Diabetes Care. 2019 Feb 22. pii: dc181510. doi: 10.2337/dc18-1510. [Epub ahead of print]

Body Composition and Diabetes Risk in South Asians: Findings From the MASALA and MESA Studies.

Author information

1
University of California, San Francisco, Department of Physiological Nursing, San Francisco, CA elena.flowers@ucsf.edu.
2
University of California, San Francisco, Institute for Human Genetics, San Francisco, CA.
3
University of California, San Francisco, Department of Epidemiology and Biostatistics, San Francisco, CA.
4
Northwestern University Feinberg School of Medicine, Department of Medicine, Chicago, IL.
5
University of California, San Diego, Department of Family Medicine and Public Health, San Diego, CA.
6
Vanderbilt University, Department of Radiology and Radiological Sciences, Nashville, TN.
7
Wake Forest School of Medicine, Department of Internal Medicine, Section of Gerontology and Geriatric Medicine, Winston-Salem, NC.
8
Massachusetts General Hospital, Division of Cardiology, Boston, MA.
9
Northwestern University Feinberg School of Medicine, Department of Preventive Medicine, Chicago, IL.
10
Wake Forrest University, Department of Internal Medicine, Section on Cardiovascular Medicine, Winston-Salem, NC.
11
University of California, San Francisco, Department of Medicine, Division of General Internal Medicine, San Francisco, CA.

Abstract

OBJECTIVE:

South Asians have a higher prevalence of type 2 diabetes compared with other race/ethnic groups. Body composition is associated with the risk for type 2 diabetes. Differences in body composition between South Asians and other race/ethnic groups are one hypothesized mechanism to explain the disproportionate prevalence of type 2 diabetes in this population.

RESEARCH DESIGN AND METHODS:

This study used data from the Mediators of Atherosclerosis in South Asians Living in America (MASALA) and the Multi-Ethnic Study of Atherosclerosis (MESA) cohorts to determine whether body composition mediated the elevated prevalence of impaired fasting glucose and type 2 diabetes in South Asians. Participants (n = 2,615) with complete body composition data were included. Ordinal logistic regression models were calculated to determine the odds for glycemic impairment in South Asians compared with the MESA cohort.

RESULTS:

In multivariate models, South Asians had a significantly higher prevalence of glycemic impairment and type 2 diabetes compared with all four race/ethnic groups included in the MESA (P < 0.001 for all). In unadjusted and multivariate adjusted models, South Asians had higher odds for impaired fasting glucose and type 2 diabetes compared with all other race/ethnic groups (P < 0.001 for all). The addition of body composition measures did not significantly mitigate this relationship.

CONCLUSIONS:

We did not identify strong evidence that accounting for body composition explains differences in the risk for type 2 diabetes. Future prospective studies of the MESA and MASALA cohorts are needed to understand how adipose tissue impacts the risk for type 2 diabetes and how to best assess this risk.

PMID:
30796111
DOI:
10.2337/dc18-1510
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20.
Diabetes Care. 2019 Apr;42(4):529-538. doi: 10.2337/dc18-1732. Epub 2019 Feb 22.

Effects of Light Therapy on Mood and Insulin Sensitivity in Patients With Type 2 Diabetes and Depression: Results From a Randomized Placebo-Controlled Trial.

Author information

1
Amsterdam UMC, Vrije Universiteit, and GGZ inGeest, Department of Psychiatry, Amsterdam Public Health research institute, Amsterdam, the Netherlands a.brouwer1@vumc.nl.
2
Amsterdam UMC, Vrije Universiteit, Department of Internal Medicine, Diabetes Center, Amsterdam, the Netherlands.
3
Amsterdam UMC, Vrije Universiteit, Department of Ophthalmology, Amsterdam, the Netherlands.
4
Amsterdam UMC, Vrije Universiteit, Department of Epidemiology and Biostatistics, Amsterdam Public Health research institute, Amsterdam, the Netherlands.
5
Amsterdam UMC, Vrije Universiteit, Department of General Practice and Elderly Care Medicine, Amsterdam Public Health research institute, Amsterdam, the Netherlands.
6
Amsterdam UMC, Vrije Universiteit, and GGZ inGeest, Department of Psychiatry, Amsterdam Public Health research institute, Amsterdam, the Netherlands.
7
Netherlands Institute for Neuroscience, Department of Sleep and Cognition, Amsterdam, the Netherlands.
8
Amsterdam UMC, Vrije Universiteit, Department of Integrative Neurophysiology, Centre for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, Amsterdam, the Netherlands.
9
Amsterdam UMC, Vrije Universiteit and University of Amsterdam, Department of Medical Psychology, Amsterdam Public Health research institute, Amsterdam, the Netherlands.

Abstract

OBJECTIVE:

Depression is common in patients with type 2 diabetes and adversely affects quality of life and diabetes outcomes. We assessed whether light therapy, an antidepressant, improves mood and insulin sensitivity in patients with depression and type 2 diabetes.

RESEARCH DESIGN AND METHODS:

This randomized, double-blind, placebo-controlled trial included 83 patients with depression and type 2 diabetes. The intervention comprised 4 weeks of light therapy (10,000 lux) or placebo light therapy daily at home. Primary outcomes included depressive symptoms (Inventory of Depressive Symptomatology [IDS]) and insulin sensitivity (M-value derived from the results of a hyperinsulinemic-euglycemic clamp). Secondary outcomes were related psychological and glucometabolic measures.

RESULTS:

Intention-to-treat analysis showed that light therapy was not superior to placebo in reducing depressive symptoms (-3.9 IDS points [95% CI -9.0 to 1.2]; P = 0.248) and had no effect on insulin sensitivity (0.15 mg/kg*min [95% CI -0.41 to 0.70]; P = 0.608). Analyses incorporating only those participants who accurately adhered to the light therapy protocol (n = 51) provided similar results, but did suggest positive effects of light therapy on depression response rates (≥50% reduction in IDS points) (26% more response; P = 0.031). Prespecified analysis showed effect moderation by baseline insulin sensitivity (P = 0.009) and use of glucose-lowering medication (P = 0.023). Light therapy did not affect depressive symptoms in participants with higher insulin sensitivity or those who use only oral glucose-lowering medication or none at all, but it did produce a relevant effect in participants with lower insulin sensitivity (-12.9 IDS points [95% CI -21.6 to -4.2]; P = 0.017) and a trend toward effectiveness in those using insulin (-12.2 IDS points [95% CI -21.3 to -3.1]; P = 0.094). Light therapy was well tolerated.

CONCLUSIONS:

Although this trial is essentially inconclusive, secondary analyses indicate that light therapy might be a promising treatment for depression among a subgroup of highly insulin-resistant individuals with type 2 diabetes.

PMID:
30796110
DOI:
10.2337/dc18-1732
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