Disrupted Control of Xenin and Ghrelin in Night Workers
Overweight, female night workers had an appetite-stimulating profile of upper gut hormones, represented by a blunted postprandial suppression of ghrelin (an orexigenic hormone) and a blunted postprandial rise of xenin (an anorexigenic hormone), as compared with day workers matched to age, gender and BMI. Other features of these night workers included increased total body and abdominal adiposity, lower insulin sensitivity and related alterations in lipids and adipokines.
The blunted postprandial suppression of ghrelin observed is in accordance with previous studies that found increased ghrelin levels in conditions of impaired sleep and in night workers.
One novelty of this study is the description of an impairment of xenin physiology in a clinical context. The satiety and metabolic effects of xenin are described in animals. However, little is known about its role in humans. The importance of xenin is reinforced by the finding of physiologically concordant alterations in these two upper gut hormones, suggesting that they interact in the entero-hypothalamic axis.
Peripheral appetite-regulating systems, including gut hormones, are modulated by circadian rhythm and sleep–awake homeostasis through sympathetic and parasympathetic nervous activity and hypothalamic control of pituitary hormones. Night work affects sleep quality and disrupts that homeostasis, which may explain the disrupted control of xenin and ghrelin secretion.
It is possible that this appetite-stimulating profile contributes to the increased total body adiposity (fat mass percentage) and abdominal adiposity (waist circumference) in night workers through higher intake of total energy intake, lipids and carbohydrates. As expected for these features, night workers had lower insulin sensitivity and increased triglycerides and tended to have increased usCRP, an inflammatory marker.
Alternatively, the disrupted control of xenin and ghrelin could relate to the increased adiposity itself rather than to shift work. Lower levels of ghrelin are found in obesity and increase after weight loss, except for that induced by Roux-en-Y gastric bypass (RYGBP), in which ghrelin further decreases to a lowest level, as an effect of the upper gut exclusion. High levels of xenin were associated with obesity grade III and improved after RYGBP. However, a causal role for obesity in this case is not proven because xenin could be affected by the upper gut exclusion itself, like ghrelin. We attempted to limit the potential effect of obesity by matching groups by BMI within overweight range, even though night workers yet had increased body fat percentage.
Lower leptin levels have been related to shift work and impaired sleep in some studies, but not all. We found a lack of difference in leptin levels even though night workers showed greater body fat mass. One possible explanation for this finding is that the absolute difference in body fat mass could not be enough to affect the circulating levels of leptin. Alternatively, night workers could have inappropriately lower levels of leptin (relatively to fat mass) associated with neuro-hormonal dysregulation secondary to shift work.
PYY3–36, oxyntomodulin and GLP-1 were not different in the current study as well. As far as we are aware, our data on PYY3–36 and oxyntomodulin relating to shift work or sleep disorders are novel in the literature. GLP-1 was not affected in a previous study of simulated shift work.
Our study has a few limitations, none of which affects the results. First, we did not evaluate 24-h hormonal profiles. On the other hand, a dynamic hormonal profile was provided by the MTT. Second, total ghrelin was assayed rather than its active, acylated form. Nevertheless, most of the physiology of ghrelin has been defined based on the assay of total ghrelin. Third, our results are preliminary and it was not established whether night shift affected body composition through the upper gut hormones or these hormones were influenced by body composition and related metabolic profile (these latter two, in turn, could have been affected by the increased energy intake through factors other than upper gut hormones).
Night workers presented a disrupted control of ghrelin and xenin, associated with behavioural changes in diet and sleep and increased adiposity and related metabolic alterations, compared with day workers within the same BMI range. However, it is not clear whether these hormones have a causative or correlative role. Regardless of the physiopathological paths involved, shift workers should be evaluated for metabolic parameters and receive advice for lifestyle behaviour such as diet and sleep.
Discussion
Overweight, female night workers had an appetite-stimulating profile of upper gut hormones, represented by a blunted postprandial suppression of ghrelin (an orexigenic hormone) and a blunted postprandial rise of xenin (an anorexigenic hormone), as compared with day workers matched to age, gender and BMI. Other features of these night workers included increased total body and abdominal adiposity, lower insulin sensitivity and related alterations in lipids and adipokines.
The blunted postprandial suppression of ghrelin observed is in accordance with previous studies that found increased ghrelin levels in conditions of impaired sleep and in night workers.
One novelty of this study is the description of an impairment of xenin physiology in a clinical context. The satiety and metabolic effects of xenin are described in animals. However, little is known about its role in humans. The importance of xenin is reinforced by the finding of physiologically concordant alterations in these two upper gut hormones, suggesting that they interact in the entero-hypothalamic axis.
Peripheral appetite-regulating systems, including gut hormones, are modulated by circadian rhythm and sleep–awake homeostasis through sympathetic and parasympathetic nervous activity and hypothalamic control of pituitary hormones. Night work affects sleep quality and disrupts that homeostasis, which may explain the disrupted control of xenin and ghrelin secretion.
It is possible that this appetite-stimulating profile contributes to the increased total body adiposity (fat mass percentage) and abdominal adiposity (waist circumference) in night workers through higher intake of total energy intake, lipids and carbohydrates. As expected for these features, night workers had lower insulin sensitivity and increased triglycerides and tended to have increased usCRP, an inflammatory marker.
Alternatively, the disrupted control of xenin and ghrelin could relate to the increased adiposity itself rather than to shift work. Lower levels of ghrelin are found in obesity and increase after weight loss, except for that induced by Roux-en-Y gastric bypass (RYGBP), in which ghrelin further decreases to a lowest level, as an effect of the upper gut exclusion. High levels of xenin were associated with obesity grade III and improved after RYGBP. However, a causal role for obesity in this case is not proven because xenin could be affected by the upper gut exclusion itself, like ghrelin. We attempted to limit the potential effect of obesity by matching groups by BMI within overweight range, even though night workers yet had increased body fat percentage.
Lower leptin levels have been related to shift work and impaired sleep in some studies, but not all. We found a lack of difference in leptin levels even though night workers showed greater body fat mass. One possible explanation for this finding is that the absolute difference in body fat mass could not be enough to affect the circulating levels of leptin. Alternatively, night workers could have inappropriately lower levels of leptin (relatively to fat mass) associated with neuro-hormonal dysregulation secondary to shift work.
PYY3–36, oxyntomodulin and GLP-1 were not different in the current study as well. As far as we are aware, our data on PYY3–36 and oxyntomodulin relating to shift work or sleep disorders are novel in the literature. GLP-1 was not affected in a previous study of simulated shift work.
Our study has a few limitations, none of which affects the results. First, we did not evaluate 24-h hormonal profiles. On the other hand, a dynamic hormonal profile was provided by the MTT. Second, total ghrelin was assayed rather than its active, acylated form. Nevertheless, most of the physiology of ghrelin has been defined based on the assay of total ghrelin. Third, our results are preliminary and it was not established whether night shift affected body composition through the upper gut hormones or these hormones were influenced by body composition and related metabolic profile (these latter two, in turn, could have been affected by the increased energy intake through factors other than upper gut hormones).
Night workers presented a disrupted control of ghrelin and xenin, associated with behavioural changes in diet and sleep and increased adiposity and related metabolic alterations, compared with day workers within the same BMI range. However, it is not clear whether these hormones have a causative or correlative role. Regardless of the physiopathological paths involved, shift workers should be evaluated for metabolic parameters and receive advice for lifestyle behaviour such as diet and sleep.
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