Orexin-A-sensitive site for energy expenditure localized in the arcuate nucleus of the hypothalamus

Wang, Jian; Osaka, Toshimasa; Inoue, Shuji

doi:10.1016/s0006-8993(03)02437-5

Cited by 34 publications

(45 citation statements)

References 27 publications

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“…3, A and B). As expected, PPO gene expression was increased from 24 up to 96 h of sleep deprivation, but it was reduced to the control levels after the recovery period [F (6,60) ϭ 5.36, P Ͻ 0.0001; Fig. 3C].…”

Section: Table 1 Primer Sequences Used In Quantitative Pcr Reactionssupporting

confidence: 69%

“…Despite the fact that there was no change in the expression of AgRP [F (6,60) ϭ 1.34, P ϭ 0.25], the expression of NPY was increased from 48 up to 96 h of sleep deprivation, supporting the observed changes in the food intake, whereas recovery and sleep-restricted groups were similar to the control animals [F (6,60) ϭ 4.85, P Ͻ 0.001] (Fig. 3, A and B).…”

Section: Table 1 Primer Sequences Used In Quantitative Pcr Reactionsmentioning

confidence: 89%

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Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

Martins¹,

Marques²,

Tufik³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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Martins PJ, Marques MS, Tufik S, D'Almeida V. Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation. Am J Physiol Endocrinol Metab 298: E726 -E734, 2010. First published January 5, 2010 doi:10.1152/ajpendo.00660.2009.-Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. In the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. In conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance. neuropeptide Y; leptin; glucagon; insulin; liver glycogen; triacylglycerol SEVERAL PIECES OF EVIDENCE support that sleep duration plays a role in body weight control (4, 15, 56). Everson et al. (10), Kushida et al. (24), and Rechtschaffen et al. (46), using an animal model, characterized a syndrome induced in response to sleep deprivation especially composed of a progressive increase in food intake. Interestingly, Spiegel et al. (55) has shown that humans who are sleep restricted for 2 days (sleeping 4 h/night) were hungrier and developed a craving for food with a high carbohydrate content. Later, the hyperphagic behavior during sleep deprivation was attributed to an increase and decrease in the hypothalamic expression of neuropeptide Y (NPY) and proopiomelanocortin (POMC), respectively (20). Supporting such changes in these neuropeptides, earlier studies in different species have found a reduction in circulating levels of leptin in response to sleep loss (11,22,55,56). Although the d...

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Section: Table 1 Primer Sequences Used In Quantitative Pcr Reactionssupporting

confidence: 69%

Section: Table 1 Primer Sequences Used In Quantitative Pcr Reactionsmentioning

confidence: 89%

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

Martins¹,

Marques²,

Tufik³

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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“…Recent findings also suggest that dynorphin-A may play a role in the function of the orexin neurons and orexin stimulates both food intake and energy expenditure (Nakamachi et al, 2006;Wang et al, 2003). Chou et al (2001) showed that nearly all (94%) neurons of the rat lateral hypothalamic area (LHA) expressing prepro-orexin mRNA also expressed prodynorphin mRNA.…”

Section: Discussionmentioning

confidence: 99%

Reduced alcohol consumption in mice lacking preprodynorphin

Blednov

Walker

Martinez

et al. 2006

Alcohol

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Many studies suggest a role for endogenous opioid peptides and their receptors in regulation of ethanol intake. It is commonly accepted that the κ-opioid receptors and their endogenous ligands, dynorphins, produce a dysphoric state and therefore may be responsible for avoidance of alcohol. We used mutant mice lacking preprodynorphin in a variety of behavioral tests of alcohol actions. Null mutant female, but not male, mice showed significantly lower preference for alcohol and consumed lower amounts of alcohol in a two-bottle choice test as compared with wild-type littermates. In the same test, knockout mice of both sexes showed a strong reduction of preference for saccharin compared to control mice. In contrast, under conditions of limited (4 hours) access (light phase of the light/dark cycle), null mutant mice did not show any differences in consumption of saccharin but they showed significantly reduced intake of sucrose. To determine the possible cause for reduction of ethanol preference and intake, we studied other ethanol-related behaviors in mice lacking the preprodynorphin gene. There were no differences between null mutant and wild type mice in ethanol-induced loss of righting reflex, acute ethanol withdrawal, ethanol-induced conditioned place preference or conditioned taste aversion to ethanol. These results indicate that deletion of preprodynorphin leads to substantial reduction of alcohol intake in female mice, and suggest thath this is caused by decreased orosensory reward of alcohol (sweet taste and/or palatability).

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“…Therefore, increased secretion of OXA in this study may be due to low blood glucose resulted from physical activity (24,25). Recent studies indicated that OXA increased glucose uptake by elevated translocation of the glucose transporter GLUT4 from cytoplasm into the plasma membrane (25). Hence, the effects of OXA and glucose are in interaction, so that increase in OXA may cause an increase in GLUT4 activity and decrease in blood glucose, and high blood sugar may decrease the expression of OXA in brain.…”

Section: Discussionmentioning

confidence: 71%

“…Researchers reported that stimulation of OXA secretion and its role in increased desire to take food is because of reduction in glucose levels. Therefore, increased secretion of OXA in this study may be due to low blood glucose resulted from physical activity (24,25). Recent studies indicated that OXA increased glucose uptake by elevated translocation of the glucose transporter GLUT4 from cytoplasm into the plasma membrane (25).…”

Section: Discussionmentioning

confidence: 76%

Acute Aerobic Exercise and Plasma Levels of Orexin A, Insulin, Glucose, and Insulin Resistance in Males With Type 2 Diabetes

Alizadeh

Farhad

Hamid

et al. 2016

Jundishapur J Health Sci

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Background: The endocrine system disruptions are the main factors in metabolic disorders which are due to lifestyle changes, obesity, and aging. Insulin resistance is impaired glucose homeostasis in the presence of insulin and is related to many diseases such as hypertension, coronary artery disease, and type 2 diabetes Objectives: This study aimed to investigate the effect of acute aerobic exercise on plasma levels of orexin A, insulin, glucose, and insulin resistance in males with type 2 diabetes. Patients and Methods: Twenty subjects (mean age = 45.40 ± 5.42 years, mean weight = 80.91 ± 6.35 kg, body mass index = 25.41 ± 2.76 kg/ m 2 ) were randomly assigned into control and experimental groups, involving 10 people in each group. The exercise protocol consisted of one session of acute aerobic exercise on a treadmill at 60% maximal oxygen uptake and the same energy expenditure (300 kcal), which were determined by gas analyzers. Subjects were subjected to samplings before, immediately after, and 24 hours after the acute aerobic exercise. Results:The analysis of findings in P ≤ 0.05 indicated that acute aerobic exercise caused a significant increase in plasma levels of orexin A and a significant decrease in plasma levels of glucose immediately after the aerobic activity, but insignificantly affected the plasma levels of insulin and insulin resistance. Conclusions: It seems that in people with type 2 diabetes, acute aerobic exercise can decrease the plasma levels of glucose, possibly through increasing orexin A. In addition, negative energy balance is necessary to decrease the levels of insulin and insulin resistance during acute aerobic exercise.

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Orexin-A-sensitive site for energy expenditure localized in the arcuate nucleus of the hypothalamus

Cited by 34 publications

References 27 publications

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation

Reduced alcohol consumption in mice lacking preprodynorphin

Acute Aerobic Exercise and Plasma Levels of Orexin A, Insulin, Glucose, and Insulin Resistance in Males With Type 2 Diabetes

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