The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress

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The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress. / Kubrak, Olga; Koyama, Takashi; Ahrentloev, Nadja; Jensen, Line; Malita, Alina; Naseem, Muhammad Tayyib; Lassen, Mette; Nagy, Stanislav; Texada, Michael; Halberg, Kenneth; Rewitz, Kim.

In: Nature Communications, Vol. 13, 692, 2022.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kubrak, O, Koyama, T, Ahrentloev, N, Jensen, L, Malita, A, Naseem, MT, Lassen, M, Nagy, S, Texada, M, Halberg, K & Rewitz, K 2022, 'The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress', Nature Communications, vol. 13, 692. https://doi.org/10.1038/s41467-022-28268-x

APA

Kubrak, O., Koyama, T., Ahrentloev, N., Jensen, L., Malita, A., Naseem, M. T., Lassen, M., Nagy, S., Texada, M., Halberg, K., & Rewitz, K. (2022). The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress. Nature Communications, 13, [692]. https://doi.org/10.1038/s41467-022-28268-x

Vancouver

Kubrak O, Koyama T, Ahrentloev N, Jensen L, Malita A, Naseem MT et al. The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress. Nature Communications. 2022;13. 692. https://doi.org/10.1038/s41467-022-28268-x

Author

Kubrak, Olga ; Koyama, Takashi ; Ahrentloev, Nadja ; Jensen, Line ; Malita, Alina ; Naseem, Muhammad Tayyib ; Lassen, Mette ; Nagy, Stanislav ; Texada, Michael ; Halberg, Kenneth ; Rewitz, Kim. / The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress. In: Nature Communications. 2022 ; Vol. 13.

Bibtex

@article{329757643c0143b48393455755955586,
title = "The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress",
abstract = "The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the gut-derived hormones affecting metabolic and behavioral responses are poorly defined. Here we show that the endocrine cells of the Drosophila gut sense nutrient stress through a mechanism that involves the TOR pathway and in response secrete the peptide hormone allatostatin C, a Drosophila somatostatin homolog. Gut-derived allatostatin C induces secretion of glucagon-like adipokinetic hormone to coordinate food intake and energy mobilization. Loss of gut Allatostatin C or its receptor in the adipokinetic-hormone-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders.",
author = "Olga Kubrak and Takashi Koyama and Nadja Ahrentloev and Line Jensen and Alina Malita and Naseem, {Muhammad Tayyib} and Mette Lassen and Stanislav Nagy and Michael Texada and Kenneth Halberg and Kim Rewitz",
year = "2022",
doi = "10.1038/s41467-022-28268-x",
language = "English",
volume = "13",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - The gut hormone Allatostatin C/Somatostatin regulates food intake and metabolic homeostasis under nutrient stress

AU - Kubrak, Olga

AU - Koyama, Takashi

AU - Ahrentloev, Nadja

AU - Jensen, Line

AU - Malita, Alina

AU - Naseem, Muhammad Tayyib

AU - Lassen, Mette

AU - Nagy, Stanislav

AU - Texada, Michael

AU - Halberg, Kenneth

AU - Rewitz, Kim

PY - 2022

Y1 - 2022

N2 - The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the gut-derived hormones affecting metabolic and behavioral responses are poorly defined. Here we show that the endocrine cells of the Drosophila gut sense nutrient stress through a mechanism that involves the TOR pathway and in response secrete the peptide hormone allatostatin C, a Drosophila somatostatin homolog. Gut-derived allatostatin C induces secretion of glucagon-like adipokinetic hormone to coordinate food intake and energy mobilization. Loss of gut Allatostatin C or its receptor in the adipokinetic-hormone-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders.

AB - The intestine is a central regulator of metabolic homeostasis. Dietary inputs are absorbed through the gut, which senses their nutritional value and relays hormonal information to other organs to coordinate systemic energy balance. However, the gut-derived hormones affecting metabolic and behavioral responses are poorly defined. Here we show that the endocrine cells of the Drosophila gut sense nutrient stress through a mechanism that involves the TOR pathway and in response secrete the peptide hormone allatostatin C, a Drosophila somatostatin homolog. Gut-derived allatostatin C induces secretion of glucagon-like adipokinetic hormone to coordinate food intake and energy mobilization. Loss of gut Allatostatin C or its receptor in the adipokinetic-hormone-producing cells impairs lipid and sugar mobilization during fasting, leading to hypoglycemia. Our findings illustrate a nutrient-responsive endocrine mechanism that maintains energy homeostasis under nutrient-stress conditions, a function that is essential to health and whose failure can lead to metabolic disorders.

U2 - 10.1038/s41467-022-28268-x

DO - 10.1038/s41467-022-28268-x

M3 - Journal article

C2 - 35121731

VL - 13

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 692

ER -

ID: 291608829