Habitual late sleep initiation is associated with increased incidence of type 2 diabetes mellitus in Korean adults: the Korean Genome and Epidemiology Study

Abstract Study Objectives Although sleep duration and quality were significant risk factors of type 2 diabetes (T2D), the impact of sleep initiation time on the development of T2D has not been studied in large longitudinal studies. Methods A total of 3689 participants without diabetes aged 40–69 years at baseline were enrolled from the Korean Genome and Epidemiology Study and followed up for 12 years. Participants were categorized based on habitual sleep initiation time by questionnaire as follows: 20:00–22:59 (early sleepers, ES, n = 766), 23:00–00:59 (usual sleepers, US, n = 2407), and 1:00–5:59 (late sleepers, LS, n = 516). Incident T2D was identified biennially by fasting plasma glucose or 2-hour glucose after 75-g oral glucose loading or use of anti-diabetes medication. Results During follow-up, 820 cases of T2D were documented and the LS group showed the highest increase in insulin resistance. Hazard ratio (HR) (95% confidence interval) for T2D of LS compared to ES was 1.34 (1.04–1.74) after adjustment for covariates including sleep duration. The impact of late sleep on the development of T2D was more evident in older individuals (≥65 years at baseline) (HR = 4.24 [1.42–12.68] in older LS vs. older ES, HR = 1.27 [1.00–1.62] in younger LS vs. younger ES, pinteraction = 0.002). In addition, LS with low insulin secretion and sensitivity showed an approximately fivefold increased risk for T2D compared to ES with high insulin secretion and sensitivity. Conclusions/Interpretation Habitual late sleep initiation is a significant risk factor for T2D in Koreans, especially in people with lower insulin sensitivity, lower β-cell function, and older age.

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Microbiota-related metabolites and the risk of type 2 diabetes

10.2337/dc20-1234/suppl.12009102 ◽

2020 ◽

Author(s):

Jagadish Vangipurapu ◽

Lilian Fernandes Silva ◽

Teemu Kuulasmaa ◽

Ulf Smith ◽

Markku Laakso

Keyword(s):

Type 2 Diabetes ◽

Insulin Secretion ◽

Insulin Sensitivity ◽

Oral Glucose ◽

Microbial Metabolites ◽

Cross Sectional ◽

Metabolomics Data ◽

Incident Type ◽

Increased Risk

OBJECTIVE: Recent studies have highlighted the significance of microbiome in human health and disease. Changes in the metabolites produced by microbiota have been implicated in several diseases. Our objective was to identify microbiome metabolites that are associated with type 2 diabetes. RESEARCH DESIGN AND METHODS: 5,181 participants from the cross-sectional METabolic Syndrome In Men (METSIM) study that included Finnish men (age 57 ± 7 years, body mass index 26.5 ± 3.5 kg/m2) having metabolomics data available were included in our study. Metabolomics analysis was performed based on fasting plasma samples. Based on an oral glucose tolerance test, Matsuda ISI and Disposition index were calculated as markers of insulin sensitivity and insulin secretion. A total of 4,851 participants had a 7.4-year follow-up visit and 522 participants developed type 2 diabetes. RESULTS: Creatine, 1-palmitoleoylglycerol(16:1), urate, 2-hydroxybutyrate/2-hydroxyisobutyrate, xanthine, xanthurenate, kynurenate, 3-(4-hydroxyphenyl)lactate, 1-oleoylglycerol(18:1), 1-myristoylglycerol(14:0), dimethylglycine and 2-hydroxyhippurate(salicylurate) were significantly associated with an increased risk of type 2 diabetes. These metabolites were associated with decreased insulin secretion or insulin sensitivity or both. Among the metabolites that were associated with a decreased risk of type 2 diabetes, 1-linoleoyl-glycerophosphocholine (18:2) significantly reduced the risk of type 2 diabetes. CONCLUSIONS: Several novel and previously reported microbial metabolites related to gut microbiota were associated with an increased risk of incident type 2 diabetes, and they were also associated with decreased insulin secretion and insulin sensitivity. Microbial metabolites are important biomarkers for the risk of type 2 diabetes.

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Association between sleep duration and mortality risk among adults with type 2 diabetes: a prospective cohort study

Diabetologia ◽

10.1007/s00125-020-05214-4 ◽

2020 ◽

Vol 63 (11) ◽

pp. 2292-2304 ◽

Cited By ~ 1

Author(s):

Yafeng Wang ◽

Wentao Huang ◽

Adrienne O’Neil ◽

Yutao Lan ◽

Dagfinn Aune ◽

...

Keyword(s):

Type 2 Diabetes ◽

Sleep Duration ◽

Mortality Risk ◽

Oral Glucose ◽

Glucose Lowering ◽

Younger Age ◽

Increased Risk ◽

The Relationship ◽

Cvd Mortality

Abstract Aims/hypothesis This study aimed to investigate whether the effects of sleep duration interacted with the presence of diabetes. We specifically sought to examine the relationship between sleep duration and all-cause and cause-specific mortality in people with type 2 diabetes across sex, age at diagnosis, duration of diabetes and treatment type. Methods The sample consisted of 273,029 adults, including 248,817 without diabetes and 24,212 with type 2 diabetes, who participated in the National Health Interview Survey from 2004 to 2013 and whose data were linked to a mortality database up to 31 December 2015. Sleep duration was measured using self-report, whereby participants were asked ‘on average how long do you sleep each day (≤5, 6, 7, 8, 9 or ≥10 h/day)?’ The relationship between sleep duration and mortality risk was investigated using Cox proportional hazards regression model, with adjustments for demographics, BMI, lifestyle behaviours and clinical variables. Results Absolute mortality rate was higher in adults with diabetes and extremes of sleep duration (≤5 h/day, 215.0 per 10,000 person-years; ≥10 h/day, 363.5 per 10,000 person-years). There was a non-significant interaction between sleep duration and the presence of diabetes (p for interaction = 0.08). A J-shaped relationship existed between sleep duration and all-cause mortality risk in people with type 2 diabetes. Compared with the reference group (7 h/day), both shorter and longer sleep durations were associated with increased risk of all-cause mortality (≤5 h/day, HR 1.24 [95% CI 1.09, 1.40]; 6 h/day, HR 1.13 [1.01, 1.28]; 8 h/day, HR 1.17 [1.06, 1.30]; ≥10 h/day, HR 1.83 [1.61, 2.08]). Similar associations were also observed for mortality risk from CVD, cancer, kidney disease, Alzheimer’s disease and chronic lower respiratory diseases. Longer sleep duration in those with a younger age at diabetes onset was associated with greater risks of all-cause and CVD mortality. Shorter sleep duration in individuals treated with both insulin and oral glucose-lowering medication was also associated with higher risks of all-cause and CVD mortality. Conclusions/interpretation The associations between sleep duration and mortality risk may be different between diabetic and non-diabetic individuals. In people with type 2 diabetes, sleeping less or more than 7 h/day was associated with increased risk of all-cause and condition-specific mortality. The association was more prominent in those with a younger age at diabetes onset and receiving treatment with both oral glucose-lowering medication and insulin. This population may benefit from targeted sleep-related interventions to reduce the risks of adverse health outcomes.

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Microbiota-related metabolites and the risk of type 2 diabetes

10.2337/dc20-1234/suppl.12009102.v1 ◽

2020 ◽

Cited By ~ 1

Author(s):

Jagadish Vangipurapu ◽

Lilian Fernandes Silva ◽

Teemu Kuulasmaa ◽

Ulf Smith ◽

Markku Laakso

Keyword(s):

Type 2 Diabetes ◽

Insulin Secretion ◽

Insulin Sensitivity ◽

Oral Glucose ◽

Microbial Metabolites ◽

Cross Sectional ◽

Metabolomics Data ◽

Incident Type ◽

Increased Risk

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The Expression of Aldolase B in Islets Is Negatively Associated With Insulin Secretion in Humans

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2018-00791 ◽

2018 ◽

Vol 103 (12) ◽

pp. 4373-4383 ◽

Cited By ~ 13

Author(s):

Felicia Gerst ◽

Benjamin A Jaghutriz ◽

Harald Staiger ◽

Anke M Schulte ◽

Estela Lorza-Gil ◽

...

Keyword(s):

Gene Expression ◽

Type 2 Diabetes ◽

Insulin Secretion ◽

Oral Glucose ◽

Gene Variants ◽

Mrna Levels ◽

Hyperglycemic Clamp ◽

Increased Risk

Abstract Context Reduced β-cell mass, impaired islet function, and dedifferentiation are considered causal to development of hyperglycemia and type 2 diabetes. In human cohort studies, changes of islet cell–specific expression patterns have been associated with diabetes but not directly with in vivo insulin secretion. Objective This study investigates alterations of islet gene expression and corresponding gene variants in the context of in vivo glycemic traits from the same patients. Methods Fasting blood was collected before surgery, and pancreatic tissue was frozen after resection from 18 patients undergoing pancreatectomy. Islet tissue was isolated by laser capture microdissection. Islet transcriptome was analyzed using microarray and quantitative RT-PCR. Proteins were examined by immunohistochemistry and western blotting. The association of gene variants with insulin secretion was investigated with oral glucose tolerance test (OGTT)-derived insulin secretion measured in a large cohort of subjects at increased risk of type 2 diabetes and with hyperglycemic clamp in a subset. Results Differential gene expression between islets from normoglycemic and hyperglycemic patients was prominent for the glycolytic enzyme ALDOB and the obesity-associated gene FAIM2. The mRNA levels of both genes correlated negatively with insulin secretion and positively with HbA1c. Islets of hyperglycemic patients displayed increased ALDOB immunoreactivity in insulin-positive cells, whereas α- and δ-cells were negative. Exposure of isolated islets to hyperglycemia augmented ALDOB expression. The minor allele of the ALDOB variant rs550915 associated with significantly higher levels of C-peptide and insulin during OGTT and hyperglycemic clamp, respectively. Conclusion Our analyses suggest that increased ALDOB expression in human islets is associated with lower insulin secretion.

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Sarcopenic phenotypes are associated with an increased risk of type 2 diabetes: findings from the Korean Genome and Epidemiology Study (KoGES)

Endocrine Abstracts ◽

10.1530/endoabs.65.p167 ◽

2019 ◽

Author(s):

Jang Won Son ◽

Won Young Lee ◽

Soon Jib Yoo

Keyword(s):

Type 2 Diabetes ◽

Epidemiology Study ◽

Increased Risk

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CANCER OF THE ORGANS OF THE REPRODUCTIVE SYSTEM IN WOMEN WITH TYPE 2 DIABETES. EFFECTS OF ANTIDIABETIC THERAPY

Wiadomości Lekarskie ◽

10.36740/wlek202005124 ◽

2020 ◽

Vol 73 (5) ◽

pp. 967-971

Author(s):

Tamara S. Vatseba

Keyword(s):

Type 2 Diabetes ◽

Combination Therapy ◽

Postmenopausal Women ◽

Reproductive System ◽

Uterine Cancer ◽

Antidiabetic Therapy ◽

Increased Risk ◽

Risk Of Cancer ◽

The Impact

The aim: to investigate the prevalence of cancer of the reproductive system in women with type 2 diabetes, and to examine the impact of antidiabetic therapy on cancer risk of this localization. Materials and methods: The study included a retrospective analysis of medical records of women with T2D with first diagnosed cancer during 2012-2016. The bases for the study were specialized medical institutions in Ivano-Frankivsk region. The obtained results were processed using statistical programs “Microsoft Excel” and “Statistika-12”. Results: Breast, uterine, and ovarian cancer were detected in 202 postmenopausal women, 63.92% from the total number of cancer cases in women. An increased risk of breast [OR = 1.24; 95% CI (1.04 – 1.50) P = 0.019] and uterine cancer [OR = 1.32; 95% CI (1.02 – 1.69) P = 0.040] has been identified. Most often, before the detection of cancer, women received combination therapy with sulfonylurea and metformin (83 patients (57.64%)) with BMI 32.64 ± 3.69 kg/m2. The difference between risk of cancer on metformin monotherapy and on sulfonylurea monotherapy [OR = 2.17; 95% CI (0.88 – 5.36) P = 0.141] or on combination therapy [OR = 1.68; 95% CI (0.76 – 3.74) P = 0.276] was not found. Conclusions: Postmenopausal women have an increased risk of breast and uterine cancer and are recommended to be screened for these diseases

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Obstructive Sleep Apnoea and Type 2 Diabetes

US Endocrinology ◽

10.17925/use.2014.10.01.35 ◽

2014 ◽

Vol 10 (01) ◽

pp. 35 ◽

Cited By ~ 1

Author(s):

Abd A Tahrani ◽

Asad Ali ◽

◽

Keyword(s):

Type 2 Diabetes ◽

Risk Factor ◽

Medical Condition ◽

Diabetes Type 2 ◽

Sleep Apnoea ◽

Obstructive Sleep ◽

Increased Risk ◽

Osa Treatment ◽

The Impact

With the growing prevalence of obesity, the burden of type 2 diabetes is increasing. Obstructive sleep apnea (OSA) is a very common medical condition that is associated with increased risk for cardiovascular disease and mortality. Obesity is a common risk factor for OSA and type 2 diabetes and hence it is not surprising that OSA and type 2 diabetes are interlinked. OSA has been shown to be an independent risk factor for the development of incident pre-diabetes/type 2 diabetes. OSA is also associated with worse glycemic control and vascular disease in patients with type 2 diabetes. However, evidence for the benefits of OSA treatment in patients with type 2 diabetes is still lacking. The aim of this article is to provide an overview of OSA, the relationships between OSA and dysglycemia and the impact of OSA in patients with type 2 diabetes, highlighting recent advances in the field.

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Interplay of Dinner Timing and MTNR1B Type 2 Diabetes Risk Variant on Glucose Tolerance and Insulin Secretion: A Randomized Crossover Trial

10.2337/figshare.17122142 ◽

2022 ◽

Author(s):

Marta Garaulet ◽

Jesus Lopez-Minguez ◽

Hassan S Dashti ◽

Céline Vetter ◽

Antonio Miguel Hernández-Martínez ◽

...

Keyword(s):

Type 2 Diabetes ◽

Insulin Secretion ◽

Glucose Tolerance ◽

Area Under The Curve ◽

Serum Levels ◽

Postprandial Glucose ◽

Oral Glucose ◽

Elevated Concentration ◽

Endogenous Melatonin

Objective: We tested whether the concurrence of food intake and elevated concentration of endogenous melatonin, as occurs in late eating, results in impaired glucose control, in particular in carriers of the type 2 diabetes-associated G allele in the melatonin-receptor-1-b gene (MTNR1B). Research Design and Methods: In a Spanish natural late eating population, a randomized, cross-over study design was performed, following an 8-h fast. Each participant (n=845) underwent two evening 2-h 75g oral glucose tolerance tests (OGTT): an early condition scheduled 4 hours prior to habitual bedtime (“early dinner-timing”), and a late condition scheduled 1 hour prior to habitual bedtime (“late dinner-timing”), simulating an early and a late dinner timing, respectively. Differences in postprandial glucose and insulin responses were determined using incremental area under the curve (AUC) calculated by the trapezoidal method between early and late dinner-timing. Results: Melatonin serum levels were 3.5-fold higher in the late vs. early condition, with late dinner-timing resulting in 6.7% lower insulin area-under-the-curve (AUC) and 8.3% higher glucose AUC. In the late condition MTNR1B G-allele carriers had lower glucose tolerance than non-carriers. Genotype differences in glucose tolerance were attributed to reductions in β-cell function (Pint AUCgluc=0.009, Pint CIR=0.022, Pint DI=0.018). Conclusions: Concurrently high endogenous melatonin and carbohydrate intake, as typical for late eating, impair glucose tolerance, especially in MTNR1B G-risk-allele carriers, attributable to insulin secretion defects.

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The SLC16A11 Risk Haplotype for Type 2 Diabetes (T2D) Is Associated to Differentiated Responses in Weight Loss, and Glucose Metabolism After Treatments to Prevent T2D

Current Developments in Nutrition ◽

10.1093/cdn/nzaa058_033 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 1275-1275

Author(s):

Magdalena Sevilla ◽

Donaji Gomez-Velasco ◽

Ivette Cruz-Bautista ◽

Laura Lazaro-Carrera ◽

Paloma Almeda-Valdes ◽

...

Keyword(s):

Type 2 Diabetes ◽

Weight Loss ◽

Area Under The Curve ◽

Postprandial Glucose ◽

Tolerance Test ◽

Oral Glucose ◽

Prolonged Release ◽

Risk Haplotype ◽

The Impact

Abstract Objectives A haplotype in SLC16A11 is associated with decreased insulin action, and risk for type 2 diabetes (T2D) in Mexicans. We aim to determine the impact of the risk haplotype on SLC16A11 on early therapeutic responses in treatments to prevent T2D. Methods We recruited subjects with at least one prediabetes criteria according to the American Diabetes Association, and body mass index 25–45 kg/m2. Subjects were randomized in two groups: lifestyle intervention (LSI): hypocaloric diet, 25 kcal/kg of ideal weight, 45% of the total intake of carbohydrates, 30% lipids and 15% protein sources + physical activity (>150 min medium intensity per week), or LSI + metformin (750 mg prolonged release twice a day). Interventions were prescribed by standardized dietitians. The goal was to achieve >3% weight loss. We evaluated the early treatment response in a follow-up period of 12 weeks with intermediate visits each 3 weeks to reinforce knowledge and treatment goals. Evaluations (baseline and post-treatment) included an oral glucose tolerance test (OGTT), and dual-energy X-ray absorptiometry. Adherence to treatment was measured trough electronic recordings. Participants were genotyped for the risk allele rs13342232. Researchers remained blinded to the genotype results. The effects of the risk haplotype were evaluated with linear and logistic regressions adjusted by age, sex, and baseline body fat %. Results We evaluated 61 subjects, 30 carriers, and 31 non-carriers. Most of participants (57%) achieved ≥3% weight loss. The LSI + metformin treatment increased in carriers, 2 times OR 3 IC95% (1.07 – 8.6) (P = 0.04) the probability to reach the ≥3% weight loss goal compared with LSI and non-carriers. In the same treatment, carriers had a greater decrease in the total and incremental area under the curve of insulin in the OGTT IC95% (−1.75 −0.11) (P = 0.02) compared with non-carriers and LSI. Carriers also had higher decrease in postprandial glucose compared with non-carriers regardless of treatment −12.63 + 30.38 vs 0.71 30.24 (P = 0.02). Conclusions After 12 weeks of treatment, carriers with prediabetes showed a higher probability achieve weight loss and to improve insulin secretion with metformin. Regardless of the treatment, carriers were prone to improve postprandial glucose. Funding Sources Miguel Aleman Medical Research Award.

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The impact of dietary protein restriction on insulin secretion and action

Proceedings of The Nutrition Society ◽

10.1017/s0029665199000841 ◽

1999 ◽

Vol 58 (3) ◽

pp. 647-653 ◽

Cited By ~ 6

Author(s):

Mark J. Holness

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Insulin Secretion ◽

Insulin Action ◽

Synergistic Effects ◽

Protein Restriction ◽

Dependent Diabetes Mellitus ◽

Organ Systems ◽

The Impact

The goal of this review is to develop the hypothesis, and review the evidence, that protein restriction, through synergistic effects on multiple organ systems predisposes to loss of normal regulation of fuel homeostasis that plays the central role in the development of type 2 (non-insulin-dependent) diabetes mellitus. The ability of insulin to regulate glucose production and disposal varies between individuals. These differences, together with the various compensatory mechanisms that are invoked to attempt to normalize fuel homeostasis, are of fundamental importance in the development and clinical course of type 2 diabetes mellitus. Protein deprivation impacts on both insulin secretion and insulin action. These effects may persist even when a diet containing adequate protein is presented subsequently. Data are presented that suggest that protein restriction results in an impaired ability of pancreatic β-cells to compensate adequately for the defect in insulin action in insulin-resistant individuals. This persistent impairment of insulin secretion resulting from protein restriction predisposes to loss of glucoregulatory control and impaired insulin action after the subsequent imposition of a diabetogenic challenge. This inability to maintain the degree of compensatory hyperinsulinaemia necessary to prevent loss of glucose tolerance may have relevance to the increased incidence of diabetes on changing from a nutritionally-poor diet to a Western diet, and to the hypothesis that some cases of type 2 diabetes in adulthood may be related to poor early nutrition.

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