Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds

Susanna Cirera Salicio; M. S. Jensen; V. S. Elbrønd; S. G. Moesgaard; B. O. Christoffersen; Haja Kadarmideen; Kerstin Skovgaard; Camilla Vibeke Sichlau Bruun; Peter Karlskov-Mortensen; Claus Bøttcher Jørgensen; Merete Fredholm

doi:10.1111/age.12082

Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds

Susanna Cirera Salicio, M. S. Jensen, V. S. Elbrønd, S. G. Moesgaard, B. O. Christoffersen, Haja Kadarmideen, Kerstin Skovgaard, Camilla Vibeke Sichlau Bruun, Peter Karlskov-Mortensen, Claus Bøttcher Jørgensen, Merete Fredholm

20 Citations (Scopus)

Abstract

Obesity has reached epidemic proportions globally and has become the cause of several major health risks worldwide. Presently, more than 100 loci have been related to obesity and metabolic traits in humans by genome-wide association studies. The complex genetic architecture behind obesity has triggered a need for the development of better animal models than rodents. The pig has emerged as a very promising biomedical model to study human obesity traits. In this study, we have characterized the expression patterns of six obesity-related genes, leptin (LEP), leptin receptor (LEPR), melanocortin 4 receptor (MC4R), fat mass and obesity associated (FTO), neuronal growth regulator 1 (NEGR)1 and adiponectin (ADIPOQ), in seven obesity-relevant tissues (liver; muscle; pancreas; hypothalamus; and retroperitoneal, subcutaneous and mesenteric adipose tissues) in two pig breeds (production pigs and Göttingen minipigs) that deviate phenotypically and genetically from each other with respect to obesity traits. We observe significant differential expression for LEP, LEPR and ADIPOQ in muscle and in all three adipose tissues. Interestingly, in pancreas, LEP expression is only detected in the fat minipigs. FTO shows significant differential expression in all tissues analyzed, and NEGR1 shows significant differential expression in muscle, pancreas, hypothalamus and subcutaneous adipose tissue. The MC4R transcript can be detected only in hypothalamus. In general, the expression profiles of the investigated genes are in accordance with those observed in human studies. Our study shows that both the differences between the investigated breeds and the phenotypic state with respect to obesity/leanness play a large role for differential expression of the obesity-related genes.

Original language	English
Journal	Animal Genetics
Volume	45
Issue number	1
Pages (from-to)	59-66
Number of pages	8
ISSN	0268-9146
DOIs	https://doi.org/10.1111/age.12082
Publication status	Published - Feb 2014

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1111/age.12082

Expression studies of six human obesity-related genes in seven tissues from divergent pig breedsSubmitted manuscript, 1.02 MB

Cite this

Cirera Salicio, S., Jensen, M. S., Elbrønd, V. S., Moesgaard, S. G., Christoffersen, B. O., Kadarmideen, H., Skovgaard, K., Bruun, C. V. S., Karlskov-Mortensen, P., Jørgensen, C. B., & Fredholm, M. (2014). Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds. Animal Genetics, 45(1), 59-66. https://doi.org/10.1111/age.12082

@article{ed9883554bbd435c83f2f3458c2abf98,

title = "Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds",

abstract = "Obesity has reached epidemic proportions globally and has become the cause of several major health risks worldwide. Presently, more than 100 loci have been related to obesity and metabolic traits in humans by genome-wide association studies. The complex genetic architecture behind obesity has triggered a need for the development of better animal models than rodents. The pig has emerged as a very promising biomedical model to study human obesity traits. In this study, we have characterized the expression patterns of six obesity-related genes, leptin (LEP), leptin receptor (LEPR), melanocortin 4 receptor (MC4R), fat mass and obesity associated (FTO), neuronal growth regulator 1 (NEGR)1 and adiponectin (ADIPOQ), in seven obesity-relevant tissues (liver; muscle; pancreas; hypothalamus; and retroperitoneal, subcutaneous and mesenteric adipose tissues) in two pig breeds (production pigs and G{\"o}ttingen minipigs) that deviate phenotypically and genetically from each other with respect to obesity traits. We observe significant differential expression for LEP, LEPR and ADIPOQ in muscle and in all three adipose tissues. Interestingly, in pancreas, LEP expression is only detected in the fat minipigs. FTO shows significant differential expression in all tissues analyzed, and NEGR1 shows significant differential expression in muscle, pancreas, hypothalamus and subcutaneous adipose tissue. The MC4R transcript can be detected only in hypothalamus. In general, the expression profiles of the investigated genes are in accordance with those observed in human studies. Our study shows that both the differences between the investigated breeds and the phenotypic state with respect to obesity/leanness play a large role for differential expression of the obesity-related genes.",

author = "{Cirera Salicio}, Susanna and Jensen, {M. S.} and Elbr{\o}nd, {V. S.} and Moesgaard, {S. G.} and Christoffersen, {B. O.} and Haja Kadarmideen and Kerstin Skovgaard and Bruun, {Camilla Vibeke Sichlau} and Peter Karlskov-Mortensen and J{\o}rgensen, {Claus B{\o}ttcher} and Merete Fredholm",

year = "2014",

month = feb,

doi = "10.1111/age.12082",

language = "English",

volume = "45",

pages = "59--66",

journal = "Animal Genetics",

issn = "0268-9146",

publisher = "Wiley-Blackwell",

number = "1",

}

TY - JOUR

T1 - Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds

AU - Cirera Salicio, Susanna

AU - Jensen, M. S.

AU - Elbrønd, V. S.

AU - Moesgaard, S. G.

AU - Christoffersen, B. O.

AU - Kadarmideen, Haja

AU - Skovgaard, Kerstin

AU - Bruun, Camilla Vibeke Sichlau

AU - Karlskov-Mortensen, Peter

AU - Jørgensen, Claus Bøttcher

AU - Fredholm, Merete

PY - 2014/2

Y1 - 2014/2

N2 - Obesity has reached epidemic proportions globally and has become the cause of several major health risks worldwide. Presently, more than 100 loci have been related to obesity and metabolic traits in humans by genome-wide association studies. The complex genetic architecture behind obesity has triggered a need for the development of better animal models than rodents. The pig has emerged as a very promising biomedical model to study human obesity traits. In this study, we have characterized the expression patterns of six obesity-related genes, leptin (LEP), leptin receptor (LEPR), melanocortin 4 receptor (MC4R), fat mass and obesity associated (FTO), neuronal growth regulator 1 (NEGR)1 and adiponectin (ADIPOQ), in seven obesity-relevant tissues (liver; muscle; pancreas; hypothalamus; and retroperitoneal, subcutaneous and mesenteric adipose tissues) in two pig breeds (production pigs and Göttingen minipigs) that deviate phenotypically and genetically from each other with respect to obesity traits. We observe significant differential expression for LEP, LEPR and ADIPOQ in muscle and in all three adipose tissues. Interestingly, in pancreas, LEP expression is only detected in the fat minipigs. FTO shows significant differential expression in all tissues analyzed, and NEGR1 shows significant differential expression in muscle, pancreas, hypothalamus and subcutaneous adipose tissue. The MC4R transcript can be detected only in hypothalamus. In general, the expression profiles of the investigated genes are in accordance with those observed in human studies. Our study shows that both the differences between the investigated breeds and the phenotypic state with respect to obesity/leanness play a large role for differential expression of the obesity-related genes.

AB - Obesity has reached epidemic proportions globally and has become the cause of several major health risks worldwide. Presently, more than 100 loci have been related to obesity and metabolic traits in humans by genome-wide association studies. The complex genetic architecture behind obesity has triggered a need for the development of better animal models than rodents. The pig has emerged as a very promising biomedical model to study human obesity traits. In this study, we have characterized the expression patterns of six obesity-related genes, leptin (LEP), leptin receptor (LEPR), melanocortin 4 receptor (MC4R), fat mass and obesity associated (FTO), neuronal growth regulator 1 (NEGR)1 and adiponectin (ADIPOQ), in seven obesity-relevant tissues (liver; muscle; pancreas; hypothalamus; and retroperitoneal, subcutaneous and mesenteric adipose tissues) in two pig breeds (production pigs and Göttingen minipigs) that deviate phenotypically and genetically from each other with respect to obesity traits. We observe significant differential expression for LEP, LEPR and ADIPOQ in muscle and in all three adipose tissues. Interestingly, in pancreas, LEP expression is only detected in the fat minipigs. FTO shows significant differential expression in all tissues analyzed, and NEGR1 shows significant differential expression in muscle, pancreas, hypothalamus and subcutaneous adipose tissue. The MC4R transcript can be detected only in hypothalamus. In general, the expression profiles of the investigated genes are in accordance with those observed in human studies. Our study shows that both the differences between the investigated breeds and the phenotypic state with respect to obesity/leanness play a large role for differential expression of the obesity-related genes.

UR - http://www.scopus.com/inward/record.url?scp=84882458506&partnerID=8YFLogxK

U2 - 10.1111/age.12082

DO - 10.1111/age.12082

M3 - Journal article

C2 - 24033492

SN - 0268-9146

VL - 45

SP - 59

EP - 66

JO - Animal Genetics

JF - Animal Genetics

IS - 1

ER -

Expression studies of six human obesity-related genes in seven tissues from divergent pig breeds

Abstract

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this