Impact of Obstructive Sleep Apnea and Sleep Duration on Glucose Tolerance and Beta-Cell Function in Adults with Prediabetes or Untreated Type 2 Diabetes

Objective: Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. Research Design and Methods: 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m2) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models. Results: Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or <6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses. Conclusion: In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.

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Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

10.2337/figshare.13607591 ◽

2021 ◽

Author(s):

Babak Mokhlesi ◽

Ashley H. Tjaden ◽

Karla A. Temple ◽

Sharon L. Edelstein ◽

Susan Sam ◽

...

Keyword(s):

Type 2 Diabetes ◽

Obstructive Sleep Apnea ◽

Insulin Sensitivity ◽

Beta Cell ◽

Sleep Duration ◽

Beta Cell Function ◽

Cell Function ◽

Cell Responses ◽

Obstructive Sleep

Objective: Obstructive sleep apnea (OSA) is associated with insulin resistance and has been described as a risk factor for type 2 diabetes. Whether OSA adversely impacts pancreatic islet beta-cell function remains unclear. We aimed to investigate the association of OSA and short sleep duration with beta-cell function in overweight/obese adults with prediabetes or recently-diagnosed, treatment-naïve type 2 diabetes. Research Design and Methods: 221 adults (57.5% men, age 54.5±8.7 years, BMI 35.1±5.5 kg/m2) completed one week of wrist actigraphy and one night of polysomnography before undergoing a 3-h oral glucose tolerance test (OGTT) and a two-step hyperglycemic clamp. Associations of measures of OSA and actigraphy-derived sleep duration with HbA1c, OGTT-derived and clamp-derived outcomes were evaluated with adjusted regression models. Results: Mean±SD objective sleep duration by actigraphy was 6.6±1.0 hours/night. OSA defined as an apnea-hypopnea index (AHI) ≥5 events per hour was present in 89% of the participants; 20% mild, 28% moderate and 41% severe. Higher AHI was associated with higher HbA1c (p =0.007). However, OSA severity, measured by either AHI as a continuous variable or by categories of OSA severity, and sleep duration (continuous or <6 h vs. ≥6 h) were not associated with fasting glucose, 2-h glucose, insulin sensitivity or beta-cell responses. Conclusion: In this baseline cross-sectional analysis of the RISE clinical trial of adults with prediabetes or recently-diagnosed, untreated type 2 diabetes, the prevalence of OSA was high. Although some measures of OSA severity were associated with HbA1c, OSA severity and sleep duration were not associated with measures of insulin sensitivity or beta-cell responses.

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Obstructive Sleep Apnea, Glucose Tolerance, and β-Cell Function in Adults With Prediabetes or Untreated Type 2 Diabetes in the Restoring Insulin Secretion (RISE) Study

Diabetes Care ◽

10.2337/dc20-2127 ◽

2021 ◽

pp. dc202127

Author(s):

Babak Mokhlesi ◽

Ashley H. Tjaden ◽

Karla A. Temple ◽

Sharon L. Edelstein ◽

Susan Sam ◽

...

Keyword(s):

Type 2 Diabetes ◽

Obstructive Sleep Apnea ◽

Insulin Secretion ◽

Sleep Apnea ◽

Glucose Tolerance ◽

Cell Function ◽

Β Cell ◽

Obstructive Sleep ◽

Β Cell Function

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Impaired Glucose Tolerance And Pancreatic Beta Cell Function In Patients With Obstructive Sleep Apnea

10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2165 ◽

2012 ◽

Author(s):

Chenjuan Gu ◽

Min Li ◽

Qingyun Li

Keyword(s):

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Glucose Tolerance ◽

Beta Cell ◽

Impaired Glucose Tolerance ◽

Beta Cell Function ◽

Cell Function ◽

Pancreatic Beta Cell ◽

Obstructive Sleep ◽

Pancreatic Beta Cell Function

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Impact of insulin and metformin versus metformin alone on beta-cell function in youth with impaired glucose tolerance or recently diagnosed type 2 diabetes

Yearbook of Paediatric Endocrinology ◽

10.1530/ey.16.12.4 ◽

2019 ◽

Author(s):

Consortium Bai RISE

Keyword(s):

Type 2 Diabetes ◽

Glucose Tolerance ◽

Beta Cell ◽

Impaired Glucose Tolerance ◽

Beta Cell Function ◽

Cell Function

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Daytime variability of postprandial glucose tolerance and pancreatic beta-cell function using 12 hour profiles in persons with type 2 diabetes

Diabetic Medicine ◽

10.1111/j.1464-5491.2009.02949.x ◽

2009 ◽

Author(s):

R Peter ◽

G Dunseath ◽

SD Luzio ◽

R Chudleigh ◽

S Roy Choudhury ◽

...

Keyword(s):

Type 2 Diabetes ◽

Glucose Tolerance ◽

Beta Cell ◽

Beta Cell Function ◽

Cell Function ◽

Pancreatic Beta Cell ◽

Postprandial Glucose ◽

Pancreatic Beta Cell Function

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One-Hour Postload Hyperglycemia Is a Stronger Predictor of Type 2 Diabetes Than Impaired Fasting Glucose

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2015-2573 ◽

2015 ◽

Vol 100 (10) ◽

pp. 3744-3751 ◽

Cited By ~ 63

Author(s):

Teresa Vanessa Fiorentino ◽

Maria Adelaide Marini ◽

Francesco Andreozzi ◽

Franco Arturi ◽

Elena Succurro ◽

...

Keyword(s):

Type 2 Diabetes ◽

Insulin Sensitivity ◽

Glucose Tolerance ◽

Beta Cell ◽

Impaired Fasting Glucose ◽

Longitudinal Analysis ◽

Beta Cell Function ◽

Cell Function ◽

Fasting Glucose

Context: Subjects with normal glucose tolerance (NGT) but 1-h postload glucose ≥ 155 mg/dL (NGT-1h-high) exhibit an intermediate cardiometabolic risk profile between individuals with NGT and impaired glucose tolerance (IGT). Objective: This study aimed to evaluate whether NGT-1h-high subjects have different cardiometabolic characteristics and an increased risk of type 2 diabetes compared with individuals with isolated impaired fasting glucose (IFG). Setting, Design, and Patients: A cross-sectional analysis was performed on 595 nondiabetic subjects who underwent an oral glucose tolerance test and an euglycemic hyperinsulinemic clamp in an ambulatory care setting. In addition, a longitudinal analysis was performed on 392 individuals, who were reexamined after a followup of 5.2 ± 0.9 y. Main Outcome Measures: Insulin sensitivity, beta-cell function, and risk of developing diabetes were measured. Results: Subjects with NGT-1h-high have a significant reduction of peripheral insulin sensitivity and beta-cell function, assessed by the disposition index, compared with either 1-h postload glucose < 155 mg/dL (NGT-1h-low) or IFG individuals, but not compared with IGT. Among the 392 subjects studied in the longitudinal analysis the incidence rate of type 2 diabetes over the follow-up period was 2.9, 16.7, 12.5, and 31.4% for subjects with NGT-1h-low, NGT-1h-high, IFG, and IGT, respectively. In a Cox proportional hazard regression analysis the risk of developing diabetes for NGT-1h-high subjects was 4.02 (95% confidence interval [CI] 1.06–15.26); an even higher risk (6.67; 95% CI, 2.09–21.24) was observed in subjects with IGT, but not in the isolated IFG group (1.91; 95% CI, 0.44–8.29). Conclusions: NGT-1h-high subjects exhibit a higher risk of developing diabetes than those with IFG or NGT-1h-low, likely due to decreased insulin sensitivity and beta-cell function.

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