Effect of iodide on glucose oxidation and /sup 32/P incorporation into phospholipids stimulated by different agents in dog thyroid slices

Journal Article · Wed Mar 01 00:00:00 EST 1989 · Endocrinology; (United States)

OSTI ID:6170940

Tseng, F Y; Rani, C S; Field, J B

Since iodide (I-) inhibits TSH stimulation of cAMP formation, which mediates most of the effects of the hormone, it has been assumed that this accounts for the inhibitory action of iodide on the thyroid. However, TSH stimulation of 32P incorporation into phospholipids and stimulation of thyroid metabolism by other agonists, such as carbachol, phorbol esters, and ionophore A23187, is not cAMP mediated. The present studies examined the effect of iodide on stimulation of glucose oxidation and 32P incorporation into phospholipids by TSH and other agonists to determine if the inhibition of cAMP formation was responsible for the action of iodide. Preincubation of dog thyroid slices for 1 h with iodide (10(-4) M) inhibited TSH-, (Bu)2cAMP-, carbachol-, methylene blue-, 12-O-tetradecanoyl phorbol-13-acetate-, ionophore A23187-, prostaglandin E1-, and cholera toxin-stimulated glucose oxidation. I- also inhibited the stimulation by TSH, 12-O-tetradecanoyl phorbol-13-acetate, carbachol, and ionophore A23187 of 32P incorporation into phospholipids. The inhibition was similar whether iodide was added 2 h before or simultaneously with the agonist. I- itself sometimes stimulated basal glucose oxidation, but had no effect on basal 32P incorporation into phospholipids. The effects of iodide on basal and agonist-stimulated thyroid metabolism were blocked by methimazole (10(-3) M). When dog thyroid slices were preloaded with 32PO4 or (1-14C)glucose, the iodide inhibition of agonist stimulation disappeared, suggesting that the effect of iodide involves the transport process. In conclusion, I- inhibited stimulation of glucose oxidation and 32P incorporation into phospholipids by all agonists, indicating that the effect is independent of the cAMP system and that iodide autoregulation does not only involve this system. Oxidation and organification of iodide are necessary for the inhibition.

• Research Organization: St. Luke's Episcopal Hospital, Houston, TX (USA)
• OSTI ID: 6170940
• Journal Information: Endocrinology; (United States), Vol. 124:3
• Country of Publication: United States
• Language: English

Related Subjects

63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
59 BASIC BIOLOGICAL SCIENCES
GLUCOSE
METABOLISM
IODIDES
BIOLOGICAL EFFECTS
PHORBOL ESTERS
PHOSPHOLIPIDS
BIOSYNTHESIS
TSH
AMP
CARBON 14 COMPOUNDS
CARBON DIOXIDE
DOGS
INHIBITION
METHYLENE BLUE
PHOSPHORUS 32
PROSTAGLANDINS
THYROID
TOXINS
TRACER TECHNIQUES
ALDEHYDES
AMINES
ANIMALS
ANTI-INFECTIVE AGENTS
ANTIGENS
ANTIMICROBIAL AGENTS
AZINES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BODY
CARBOHYDRATES
CARBON COMPOUNDS
CARBON OXIDES
CARCINOGENS
CHALCOGENIDES
CHLORIDES
CHLORINE COMPOUNDS
DAYS LIVING RADIOISOTOPES
DRUGS
ENDOCRINE GLANDS
ESTERS
GLANDS
HALIDES
HALOGEN COMPOUNDS
HETEROCYCLIC COMPOUNDS
HEXOSES
HORMONES
IODINE COMPOUNDS
ISOTOPE APPLICATIONS
ISOTOPES
LABELLED COMPOUNDS
LIGHT NUCLEI
LIPIDS
MAMMALS
MATERIALS
MONOSACCHARIDES
NUCLEI
NUCLEOTIDES
ODD-ODD NUCLEI
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
ORGANIC PHOSPHORUS COMPOUNDS
ORGANIC SULFUR COMPOUNDS
ORGANS
OXIDES
OXYGEN COMPOUNDS
PEPTIDE HORMONES
PHENOTHIAZINES
PHOSPHORUS ISOTOPES
PITUITARY HORMONES
RADIOISOTOPES
SACCHARIDES
SYNTHESIS
TOXIC MATERIALS
VERTEBRATES
560300* - Chemicals Metabolism & Toxicology
550501 - Metabolism- Tracer Techniques