Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Filip Ottosson

Research student

Default user image.

N1-methylnicotinamide is a signalling molecule produced in skeletal muscle coordinating energy metabolism

Author

  • Kristoffer Ström
  • David Morales-Alamo
  • Filip Ottosson
  • Anna Edlund
  • Line Hjort
  • Sine W. Jörgensen
  • Peter Almgren
  • Yuedan Zhou
  • Marcos Martin-Rincon
  • Carl Ekman
  • Alberto Pérez-López
  • Ola Ekström
  • Ismael Perez-Suarez
  • Markus Mattiasson
  • Pedro De Pablos-Velasco
  • Nikolay Oskolkov
  • Emma Ahlqvist
  • Nils Wierup
  • Lena Eliasson
  • Allan Vaag
  • Leif Groop
  • Karin G. Stenkula
  • Céline Fernandez
  • Jose A.L. Calbet
  • Hans Christer Holmberg
  • Ola Hansson

Summary, in English

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 N1-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 ~18 h of fasting and being lowest ~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.

Department/s

  • Genomics, Diabetes and Endocrinology
  • Cardiovascular Research - Hypertension
  • Diabetes - Islet Cell Exocytosis
  • Diabetes - Cardiovascular Disease
  • Neuroendocrine Cell Biology
  • Glucose Transport and Protein Trafficking
  • Ophthalmology, Lund
  • EXODIAB: Excellence of Diabetes Research in Sweden

Publishing year

2018-12-01

Language

English

Publication/Series

Scientific Reports

Volume

8

Issue

1

Document type

Journal article

Publisher

Nature Publishing Group

Topic

  • Endocrinology and Diabetes

Status

Published

Research group

  • Genomics, Diabetes and Endocrinology
  • Cardiovascular Research - Hypertension
  • Diabetes - Islet Cell Exocytosis
  • Diabetes - Cardiovascular Disease
  • Neuroendocrine Cell Biology
  • Glucose Transport and Protein Trafficking

ISBN/ISSN/Other

  • ISSN: 2045-2322