“…In another experimental study of streptozotocin‐induced diabetes in rats, compared with normal rats, diabetic rats had a lower ventilatory response to CO 2 challenge and their sleep apnoea scores were markedly increased. Furthermore, metformin (known to reduce insulin resistance) returned sleep apnoea scores to their baseline levels, supporting the idea that insulin resistance is an important factor leading to the occurrence of apnoeas in this experimental model (Ramadan et al 2006). While some clinical studies suggest that OSA patients have normal hypercapnic responses and CPAP treatment does not markedly affect hypercapnic chemosensitivity in OSA (Narkiewicz et al 1999; Spicuzza et al 2006), it should be noted that in those studies only ‘healthy’ and untreated OSA subjects were studied and diabetes was an exclusion criterion.…”
The metabolic syndrome represents a clustering of several interrelated risk factors of metabolic origin that are thought to increase cardiovascular risk. It is still uncertain whether this clustering results from multiple underlying risk factors or whether it has a single cause. One metabolic abnormality that may underlie several clinical characteristics of the metabolic syndrome is insulin resistance. This review discusses the evidence that sleep disturbances (obstructive sleep apnoea, sleep deprivation and shift work) may independently lead to the development of both insulin resistance and individual clinical components of the metabolic syndrome. The converse may also be true, in that metabolic abnormalities associated with the metabolic syndrome and insulin resistance may potentially exacerbate sleep disorders. The notion that sleep disturbances exert detrimental metabolic effects may help explain the increasing prevalence of the metabolic syndrome and insulin resistance in the general population and may have important implications for population-based approaches to combat the increasing epidemic of metabolic and cardiovascular disease.
“…In another experimental study of streptozotocin‐induced diabetes in rats, compared with normal rats, diabetic rats had a lower ventilatory response to CO 2 challenge and their sleep apnoea scores were markedly increased. Furthermore, metformin (known to reduce insulin resistance) returned sleep apnoea scores to their baseline levels, supporting the idea that insulin resistance is an important factor leading to the occurrence of apnoeas in this experimental model (Ramadan et al 2006). While some clinical studies suggest that OSA patients have normal hypercapnic responses and CPAP treatment does not markedly affect hypercapnic chemosensitivity in OSA (Narkiewicz et al 1999; Spicuzza et al 2006), it should be noted that in those studies only ‘healthy’ and untreated OSA subjects were studied and diabetes was an exclusion criterion.…”
The metabolic syndrome represents a clustering of several interrelated risk factors of metabolic origin that are thought to increase cardiovascular risk. It is still uncertain whether this clustering results from multiple underlying risk factors or whether it has a single cause. One metabolic abnormality that may underlie several clinical characteristics of the metabolic syndrome is insulin resistance. This review discusses the evidence that sleep disturbances (obstructive sleep apnoea, sleep deprivation and shift work) may independently lead to the development of both insulin resistance and individual clinical components of the metabolic syndrome. The converse may also be true, in that metabolic abnormalities associated with the metabolic syndrome and insulin resistance may potentially exacerbate sleep disorders. The notion that sleep disturbances exert detrimental metabolic effects may help explain the increasing prevalence of the metabolic syndrome and insulin resistance in the general population and may have important implications for population-based approaches to combat the increasing epidemic of metabolic and cardiovascular disease.
“…The ventilatory and metabolic results in the STZ/N model reported in this study contrast with previous studies of diabetic rodents (Ramadan et al, 2006;Saiki et al, 2005). We have previously explored parameters of altered control of ventilation in a STZ rat model of diabetes mellitus.…”
Section: Ventilatory and Metabolic Results In Diabetic Modelscontrasting
“…An alternative explanation would be a reverse causal sequence, in which dietary choices alter nocturnal respiration, independent of BMI. Acute dietary changes can alter sleep architecture in humans [11] and ventilation control in rats [12]. Such an effect could have implications for the conduct of PSG.…”
Objective
Determine whether obstructive sleep apnea (OSA) is associated with the dietary choices of obese individuals during middle- to late-childhood. It was hypothesized that OSA would be associated with increased caloric content of a dinner order, particularly with high carbohydrate food choices. Secondarily, we examined the relationships between sleep duration and dietary choices.
Methods
42 obese subjects aged 10–16.9 years participated in a cross-sectional study that involved systematic collection of sleep duration (based on actigraphy), presence and severity of obstructive sleep apnea (obstructive apnea + hypopnea index [AHI] from inpatient polysomnography) and the macronutrient content of dinners ordered from a standardized hospital menu the evening before the polysomnogram.
Results
Primary analyses using Spearman rank-order correlations found that AHI was significantly associated with total calories, as well as grams of fat and carbohydrate, but not protein. These macronutrient variables did not correlate with sleep duration across a week, nor the night before the meal. Findings were unchanged after correcting for age- and sex-adjusted BMI.
Conclusions
More severe OSA appears to be associated with an increased preference for calorie-dense foods that are high in fat and carbohydrate in a manner that is independent of degree of overweight. Although this novel finding awaits replication, it has potential implications for the clinical care of obese youth and individuals with OSA, adds to the limited data that relate sleep to dietary choices, and may have implications for OSA-related morbidity.
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