title: Porcine somatotrophin differentially down-regulates expression of the GLUT4 and fatty acid synthase genes in pig adipose tissue.
abstract: The present study was conducted to determine whether porcine somatotropin (pST) differentially regulates expression of the GLUT4 and fatty acid synthase (FAS) genes in pig adipose tissue. Three different experiments were conducted in which pigs were treated daily with different doses of pST for different time periods (7 or 14 d and from 60 to 90 kg of body wt). In these experiments, pST significantly and consistently decreased FAS mRNA levels (80%, 66% and 85%, respectively); however, GLUT4 mRNA was not affected by pST in two of the three experiments, and in the one showing an effect (Experiment 2), the decrease was less than observed for FAS (44%). Because of these results, we conducted subsequent experiments to see if the effects of pST on glucose metabolism in cultured pig adipose tissue (48 h) differed when glucose concentrations were changed from 1 to 5 mmol/L. These studies revealed that the antagonistic effect of pST on insulin action was more potent when glucose transport was saturated (5 mmol/L) than when glucose concentration limited glucose entry into the cell (1 mmol/L). In summary, these results suggest that the effects of pST on glucose transport in pig adipocytes are secondary to changes elicited by the hormone on intracellular glucose use for lipogenesis. When considered in the context of the decrease previously observed in glucose transport in pig adipocytes, the findings reported herein suggest that pST acts to decrease GLUT4 protein activity and/or distribution between the plasma membrane and the intracellular pool with little alteration in GLUT4 gene expression or total cell GLUT4 protein.
authors.affiliation: Department of Dairy and Animal Science, The Pennsylvania State University, University Park 16802, USA.
authors.forename: S S
authors.initials: SS
authors.lastname: Donkin
authors.forename: P Y
authors.initials: PY
authors.lastname: Chiu
authors.forename: D
authors.initials: D
authors.lastname: Yin
authors.forename: I
authors.initials: I
authors.lastname: Louveau
authors.forename: B
authors.initials: B
authors.lastname: Swencki
authors.forename: J
authors.initials: J
authors.lastname: Vockroth
authors.forename: C M
authors.initials: CM
authors.lastname: Evock-Clover
authors.forename: J L
authors.initials: JL
authors.lastname: Peters
authors.forename: T D
authors.initials: TD
authors.lastname: Etherton
mesh_terms: D000199:Actins / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D000273:Adipose Tissue / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D015152:Blotting, Northern; D046508:Culture Techniques; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D064429:Fatty Acid Synthases / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D005947:Glucose / Q000378:metabolism; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D013006:Growth Hormone / Q000494:pharmacology*; D009004:Monosaccharide Transport Proteins / Q000032:analysis / Q000235:genetics* / Q000378:metabolism; D009124:Muscle Proteins; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D013552:Swine / Q000235:genetics* / Q000378:metabolism
chemical_list: D000199:Actins; D051272:Glucose Transporter Type 1; D051275:Glucose Transporter Type 4; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D012333:RNA, Messenger; D013006:Growth Hormone; D064429:Fatty Acid Synthases; D005947:Glucose