PMID- 3371552
OWN - NLM
STAT- MEDLINE
DCOM- 19880701
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 56
IP  - 3
DP  - 1988 Apr
TI  - Effect of butyrate on thyroid hormone-mediated gene expression in rat pituitary 
      tumour cells.
PG  - 263-70
AB  - These studies correlate the effects of (sodium) butyrate on intranuclear thyroid 
      hormone receptor levels, with influences on both endogenous and transfected rat 
      growth hormone (rGH) gene expression and regulation by L-triiodothyronine (T3). 
      In rat anterior pituitary tumour (GH3) cells, 5.0 mM butyrate elicits a biphasic 
      reduction in the number of nuclear T3 receptors. About 75% are depleted rapidly 
      (t1/2 = 7 h), and the remaining receptors are depleted more slowly (t1/2 = 59 h). 
      GH3 cells were treated with increasing concentrations of butyrate (0-5.0 mM), 
      plus or minus 10 nM T3 for 48 h. Total cytoplasmic RNA, cellular protein and 
      medium were analysed for rGH levels with radiolabelled rGH cDNA or antibodies. A 
      greater than 50-fold increase in rGH mRNA level was seen after T3 treatment in 
      the absence or presence of 0.1 mM butyrate. However, 1.0 and 5.0 mM butyrate 
      decreased the stimulation of rGH mRNA levels by T3 to 10- and less than 2-fold, 
      respectively. Control mRNA levels were decreased slightly by increasing butyrate 
      concentrations; rGH mRNA level was 2- to 3-fold higher in the absence of 5 mM 
      butyrate. The pattern of butyrate/T3 response displayed by both cellular and 
      secreted rGH was similar to that seen with mRNA levels. Thus, the predominant 
      effect of butyrate on T3-mediated regulation of growth hormone gene expression is 
      at the level of transcription or mRNA accumulation. A hybrid gene containing 
      5'-flanking DNA from the rGH gene fused to the bacterial gene coding for 
      chloramphenicol acetyl transferase (CAT), was used to transfect rat pituitary 
      tumour cells with or without butyrate and T3 treatments.(ABSTRACT TRUNCATED AT 
      250 WORDS)
FAU - Cattini, P A
AU  - Cattini PA
AD  - Department of Physiology, University of Manitoba, Winnipeg, Canada.
FAU - Kardami, E
AU  - Kardami E
FAU - Eberhardt, N L
AU  - Eberhardt NL
LA  - eng
GR  - 17838/PHS HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Butyrates)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Recombinant Proteins)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - 107-92-6 (Butyric Acid)
RN  - 9002-72-6 (Growth Hormone)
SB  - IM
MH  - Animals
MH  - Butyrates/*pharmacology
MH  - Butyric Acid
MH  - Gene Expression Regulation/drug effects
MH  - Growth Hormone/biosynthesis/*genetics
MH  - Pituitary Gland, Anterior
MH  - Pituitary Neoplasms/*metabolism
MH  - Protein Biosynthesis
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Receptors, Thyroid Hormone/*metabolism
MH  - Recombinant Proteins/biosynthesis/genetics
MH  - Triiodothyronine/*metabolism
MH  - Tumor Cells, Cultured
EDAT- 1988/04/01 00:00
MHDA- 1988/04/01 00:01
CRDT- 1988/04/01 00:00
PHST- 1988/04/01 00:00 [pubmed]
PHST- 1988/04/01 00:01 [medline]
PHST- 1988/04/01 00:00 [entrez]
AID - 0303-7207(88)90069-X [pii]
AID - 10.1016/0303-7207(88)90069-x [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 1988 Apr;56(3):263-70. doi: 10.1016/0303-7207(88)90069-x.