Sleep Architecture and Glucose and Insulin Homeostasis in Obese Adolescents

Abstract

OBJECTIVESleep deprivation is associated with increased risk of adult type 2 diabetes mellitus (T2DM). It is uncertain whether sleep deprivation and/or altered sleep architecture affects glycemic regulation or insulin sensitivity or secretion. We hypothesized that in obese adolescents, sleep disturbances would associate with altered glucose and insulin homeostasis.RESEARCH DESIGN AND METHODSThis cross-sectional observational study of 62 obese adolescents took place at the Clinical and Translational Research Center and Sleep Laboratory in a tertiary care children’s hospital. Subjects underwent oral glucose tolerance test (OGTT), anthropometric measurements, overnight polysomnography, and frequently sampled intravenous glucose tolerance test (FSIGT). Hemoglobin A1c (HbA1c) and serial insulin and glucose levels were obtained, indices of insulin sensitivity and secretion were calculated, and sleep architecture was assessed. Correlation and regression analyses were performed to assess the association of total sleep and sleep stages with measures of insulin and glucose homeostasis, adjusted for confounding variables.RESULTSWe found significant U-shaped (quadratic) associations between sleep duration and both HbA1c and serial glucose levels on OGTT and positive associations between slow-wave sleep (N3) duration and insulin secretory measures, independent of degree of obesity, pubertal stage, sex, and obstructive sleep apnea measures.CONCLUSIONSInsufficient and excessive sleep was associated with short-term and long-term hyperglycemia in our obese adolescents. Decreased N3 was associated with decreased insulin secretion. These effects may be related, with reduced insulin secretory capacity leading to hyperglycemia. We speculate that optimizing sleep may stave off the development of T2DM in obese adolescents.

The puzzle of metabolic effects of obstructive sleep apnoea in children

“…The data indicate that both obesity and sleep fragmentation in OSA are significantly associated with altered metabolic variables, including insulin resistance and lipid profile, whereas the frequency of nocturnal respiratory events or severity of nocturnal hypoxaemia exerts a minor effect, if any. The results of this study reinforce the conclusions of studies that demonstrated a prominent role of obesity [17][18][19][20][21] and sleep structure [22,23] as determinants of alterations in insulin resistance/sensitivity in children with OSA, but are at odds with other studies indicating an independent influence of OSA [24][25][26][27][28][29][30][31].…”

Порушення Сну При Цукровому Діабеті 1-Го Типу Залежно Від Показників Добового Моніторингу Глікемії І Досягнення Цільових Рівнів Глікемії

“…Максимальная продолжительность ОВС выявлена у пациентов первой группы -6,15 [5,40; 6,43] Оригінальні дослідження /Original Researches/ ция ее мозгом уменьшается. Описанные результаты находят подтверждение в литературе об обратной зависимости между значением НbА1с и продолжи-тельностью медленноволнового сна [12][13][14]. При-веденные результаты свидетельствуют о том, что декомпенсация препятствует углублению стадий сна, поэтому в структуре сна преобладают REM-сон, а также поверхностные стадии медленного сна.…”

The Role of Genetic, Dietary and Lifestyle Factors in Pediatric Metabolic Syndrome: A Review of the Literature from Prenatal to Adolescence

“…Sleep is crucial in childhood and The focus of attention between sleep and metabolic dysfunction has shifted with more attention now concentrating on sleep architecture. Sleep architecture (sleep staging) in relation to glucose metabolism has been explored in children and adolescents, with an initial focus on those with obesity [28,46]. A recent study investigated the effect of sleep staging upon glucose tolerance, insulin sensitivity and pancreaticcell function in children and adolescents (n = 118; mean age 13.1 years; 45% boys) [82].…”