PMID- 6286369
OWN - NLM
STAT- MEDLINE
DCOM- 19821012
LR  - 20131121
IS  - 0014-9446 (Print)
IS  - 0014-9446 (Linking)
VI  - 41
IP  - 10
DP  - 1982 Aug
TI  - Thyroid hormone-carbohydrate interaction at the hepatic nuclear level.
PG  - 2671-6
AB  - We have studied the interaction between triiodothyronine (T3) and carbohydrate 
      (CHO) in the induction of hepatic lipogenic enzymes under both in vivo and in 
      vitro conditions. Our studies demonstrate a synergistic relationship between T3 
      administration and CHO feeding in the induction of these enzymes. Likewise, in 
      states characterized by CHO deprivation such as starvation and diabetes, the 
      response to T3 is also inhibited. Studies in the aging animal have documented a 
      diminished response both to CHO and to T3. Our studies suggest that T3 multiplies 
      a primary CHO-generated signal by a constant factor, and that this signal 
      declines with age. Additional studies with primary hepatocyte cultures provide 
      evidence that glucose is the main factor responsible for the induction of hepatic 
      malate dehydrogenase: decarboxylating (EC 1.1.1.40) (ME). Glucose induces ME in 
      the absence of changes in extrahepatic hormones or metabolites and in the 
      complete absence of T3. In the cultured hepatocyte system, T3 also acts as a 
      constant multiplier of the primary glucose-derived signal. Our results provide 
      further support for the thesis that the primary action of T3 at the molecular 
      level is a multiplication of other nuclear signals. The complexity of response 
      pattern to both T3 and CHO administration, however, is illustrated by recent 
      studies in which we have analyzed the translated products of total poly(A+) RNA 
      extracted from livers of rats subjected to various physiological stimuli.
FAU - Mariash, C N
AU  - Mariash CN
FAU - Oppenheimer, J H
AU  - Oppenheimer JH
LA  - eng
GR  - AM19812/AM/NIADDK NIH HHS/United States
GR  - K080AM00800/AM/NIADDK NIH 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  - United States
TA  - Fed Proc
JT  - Federation proceedings
JID - 0372771
RN  - 0 (Carbohydrates)
RN  - 0 (Insulin)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 06LU7C9H1V (Triiodothyronine)
RN  - EC 1.1.1.37 (Malate Dehydrogenase)
RN  - EC 1.1.1.40 (malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+))
RN  - EC 1.1.1.43 (Phosphogluconate Dehydrogenase)
RN  - EC 1.1.1.49 (Glucosephosphate Dehydrogenase)
RN  - EC 2.3.1.85 (Fatty Acid Synthases)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Aging
MH  - Animals
MH  - Carbohydrates/*physiology
MH  - Cell Nucleus/physiology
MH  - Enzyme Induction
MH  - Fatty Acid Synthases/biosynthesis
MH  - Glucose/physiology
MH  - Glucosephosphate Dehydrogenase/biosynthesis
MH  - Insulin/physiology
MH  - Lipid Metabolism
MH  - Liver/*physiology
MH  - Malate Dehydrogenase/biosynthesis
MH  - Phosphogluconate Dehydrogenase/biosynthesis
MH  - Rats
MH  - Receptors, Cell Surface/metabolism
MH  - Receptors, Thyroid Hormone
MH  - Starvation
MH  - Triiodothyronine/*physiology
EDAT- 1982/08/01 00:00
MHDA- 1982/08/01 00:01
CRDT- 1982/08/01 00:00
PHST- 1982/08/01 00:00 [pubmed]
PHST- 1982/08/01 00:01 [medline]
PHST- 1982/08/01 00:00 [entrez]
PST - ppublish
SO  - Fed Proc. 1982 Aug;41(10):2671-6.