Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/44467
Title: N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism
Authors: Ström, Kristoffer
Morales-Alamo, David 
Ottosson, Filip
Edlund, Anna
Hjort, Line
Jörgensen, Sine W.
Almgren, Peter
Zhou, Yuedan
Martin-Rincon, Marcos 
Ekman, Carl
Pérez-López, Alberto
Ekström, Ola
Perez-Suarez, Ismael
Mattiasson, Markus
De Pablos-Velasco, Pedro 
Oskolkov, Nikolay
Ahlqvist, Emma
Wierup, Nils
Eliasson, Lena
Vaag, Allan
Groop, Leif
Stenkula, Karin G.
Fernandez, Céline
Holmberg, Hans Christer
Hansson, Ola
Calbet, Jose A. 
UNESCO Clasification: 32 Ciencias médicas
Issue Date: 2018
Project: Viabilidad y Sostenibilidad Del Adelgazamiento Mediante Tratamiento Intensificado en Pacientes Con Sobrepeso U Obesidad: Mecanismos Neuroendocrinos y Moleculares 
Journal: Scientific Reports 
Abstract: Obesity is a major health problem, and although caloric restriction and exercise are successful strategies to lose adipose tissue in obese individuals, a simultaneous decrease in skeletal muscle mass, negatively effects metabolism and muscle function. To deeper understand molecular events occurring in muscle during weight-loss, we measured the expressional change in human skeletal muscle following a combination of severe caloric restriction and exercise over 4 days in 15 Swedish men. Key metabolic genes were regulated after the intervention, indicating a shift from carbohydrate to fat metabolism. Nicotinamide N-methyltransferase (NNMT) was the most consistently upregulated gene following the energy-deficit exercise. Circulating levels of N-1-methylnicotinamide (MNA), the product of NNMT activity, were doubled after the intervention. The fasting-fed state was an important determinant of plasma MNA levels, peaking at similar to 18 h of fasting and being lowest similar to 3 h after a meal. In culture, MNA was secreted by isolated human myotubes and stimulated lipolysis directly, with no effect on glucagon or insulin secretion. We propose that MNA is a novel myokine that enhances the utilization of energy stores in response to low muscle energy availability. Future research should focus on applying MNA as a biomarker to identify individuals with metabolic disturbances at an early stage.
URI: http://hdl.handle.net/10553/41846
ISSN: 2045-2322
DOI: 10.1038/s41598-018-21099-1
Source: Scientific Reports [ISSN 2045-2322], v. 8, article number 3016
Appears in Collections:Artículos
Unknown (1,24 MB)
Show full item record

SCOPUSTM   
Citations

7
checked on Apr 11, 2020

WEB OF SCIENCETM
Citations

8
checked on May 23, 2020

Page view(s)

4
checked on May 30, 2020

Download(s)

1
checked on May 30, 2020

Google ScholarTM

Check

Altmetric


Share



Export metadata



Items in accedaCRIS are protected by copyright, with all rights reserved, unless otherwise indicated.