Effects of Glucose and Parathyroid Hormone on the Renal Handling of Myoinositol by Isolated Perfused Dog Kidneys

Molitoris, Bruce A.; Hruska, Keith A.; Fishman, Neil O.; Daughaday, William H.

doi:10.1172/jci109403

Cited by 16 publications

(3 citation statements)

References 24 publications

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“…Although parathyroidl hormone has a maljor effect onl MI reabsorption in the kidney (19,20), we didl not detect an effect of parathyroid hormiione or libuttrvl cyclic AMP on MII uptake in the epitrochlearis muscle.…”

contrasting

confidence: 61%

Concentration of Myo-inositol in Skeletal Muscle of the Rat Occurs without Active Transport

Molitoris¹,

Karl²,

Daughaday³

1980

J. Clin. Invest.

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contrasting

confidence: 61%

Concentration of Myo-inositol in Skeletal Muscle of the Rat Occurs without Active Transport

Molitoris¹,

Karl²,

Daughaday³

1980

J. Clin. Invest.

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“…thyroid hormone on biosynthesis of inositol in the kidney (19). Additionally there have been several inquiries into changes in the biosynthetic pathway in various physiological and experimentally induced pathological states that may reflect hormonal control ofthe enzyme.…”

Section: Figurementioning

confidence: 99%

Selective hormonal control of myo-inositol biosynthesis in reproductive organs and liver of the male rat.

Hasegawa¹,

Eisenberg²

1981

Proc. Natl. Acad. Sci. U.S.A.

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myo-Inositol biosynthesis has been examined in hypophysectomized and thyroidectomized male rats. After hypophysectomy, inositol-l-phosphate synthase [IL-myo-inositol-lphosphate lyase (isomerizing), EC 5.5. 1.4] Among the many tissues capable of synthesizing myo-inositol, the testis ranks as the richest mammalian source of inositol-1-phosphate synthase [lL-myo-inositol-l-phosphate synthase, EC 5.5.1.4], the NAD+-dependent enzyme that isomerizes glucose 6-phosphate to myo-inositol 1-phosphate (1) referred to here as simply inositol 1-phosphate. Because the testis is the target organ for various hormones and is itself the site of androgen biosynthesis, we were led to inquire into possible hormonal control of inositol biosynthesis. Although there have been sporadic reports on the effects of various physiological and pathological states on the levels of free inositol and inositol-l-phosphate synthase in certain tissues (2-7), there has been no systematic study of hormonal control of the enzyme. Here we report the effect in male rats of hypophysectomy, adrenalectomy, and thyroidectomy on tissue levels of inositol-l-phosphate synthase and preliminary experiments in the reversal of these effects by gonadotropic and thyroid hormones. MATERIALS AND METHODSMale Sprague-Dawley rats weighing approximately 200 g were obtained from Taconic Farms (Germantown, NY) and maintained as follows. Normal animals received regular tap water; hypophysectomized, 5% dextrose; thyroidectomized, 1% calcium lactate; and adrenalectomized, isotonic saline. Sham-operated rats were given the same fluids; all animals received regular laboratory chow ad lib. Tissues for enzyme assay were removed and weighed immediately after killing by decapitation. Seminal vesicles were washed with cold isotonic saline after removal of seminal fluid through an incision. Brain, liver, spleen, thymus, pancreas, kidney, testis, and ventral prostate were homogenized in a Potter-Elvehjem homogenizer with 2-3 vol of 0.154 M KCI/0.2 mM dithiothreitol. Epididymis and seminal vesicles were minced and then homogenized in a Polytron homogenizer with 3-5 vol of the same solution. The homogenates were centrifuged 20 min at 27,000 X g, and the supernatants were heated at 60'C for 2 min exactly, chilled in ice, and centrifuged at 105,000 x g for 1 hr. Solid ammonium sulfate was added to 40% of saturation (0.226 g/ml). The precipitate was collected by centrifugation, dissolved in 0.6-0.7 ml of 50 mM Tris acetate, pH 7.4/0.2 mM dithiothreitol and dialyzed against the same buffer overnight. The suspension was freed of insoluble material by centrifugation and assayed for inositol-1-phosphate synthase by incubation with glucose 6-phosphate (5 mM) and NAD' (1 mM); the resulting inositol 1-phosphate was determined as inorganic phosphate by the periodate method of Barnett et al. (8). Protein was determined by the method of Lowry et al. (9), with correction for the effect ofTris.

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“…To demonstrate such a relationship one would need an experimental model with excess PTH but normal nerve calcium content, a combination that we were unable to achieve. It should be mentioned that PTH may affect phospholipid turnover (27)(28)(29)(30) and/or content (27, 3 1) of several cells. If PTH also induces changes in phospholipid metabolism of peripheral nerves, one might expect that such an action may affect nerve function.…”

Section: Discussionmentioning

confidence: 99%

Role of Parathyroid Hormone in the Decreased Motor Nerve Conduction Velocity of Chronic Renal Failure

Akmal

Massry

1990

Experimental Biology and Medicine

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Certain data support the notion that chronic exposure to excess parathyroid hormone (PTH) is associated with decreased motor nerve conduction velocity, while other studies failed to confirm such an effect. Also, chronic renal failure of 4 months duration in dogs did not elicit changes in MNCV or calcium content of nerve. These discrepancies may be due to differences in other metabolic parameters, such as degree of uremia, serum levels of calcium, phosphorus, or magnesium, and acid-base parameters, or in duration of chronic renal failure. To examine the effect of PTH on peripheral nerve function in renal failure in a more defined biochemical setting, we studied the changes in MNCV and nerve calcium content in dogs with and without excess PTH and with prolonged and similar duration of chronic renal failure (57 +/- 1.7 weeks) and comparable biochemical parameters. Dogs with chronic renal failure displayed a significant (P less than 0.01) decrease in MNCV (before renal failure, 65 +/- 1.5 m/sec; after renal failure, 49 +/- 3.5 m/sec) and marked elevation in calcium content of peripheral nerve (444 +/- 45 mg/kg dry wt). These derangements were not observed in parathyroidectomized chronic renal failure animals; MNCV before renal failure was 66 +/- 1.5 m/sec and after renal failure was 65 +/- 1.5 m/sec, and nerve calcium content after renal failure was 229 +/- 3 mg/kg dry wt. Also, parathyroidectomy of three dogs with preexisting chronic renal failure of 52 weeks was associated with reversal of the abnormalities in MNCV and calcium content of nerve despite an additional period of renal failure of 52 weeks in two of the dogs and 40 weeks in the third. Our data are consistent with the proposition that excess PTH plays a major role in the genesis of peripheral nerve dysfunction in chronic renal failure. This adverse effect of the hormone is most likely mediated by the PTH-induced accumulation of calcium in peripheral nerve.

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Effects of Glucose and Parathyroid Hormone on the Renal Handling of Myoinositol by Isolated Perfused Dog Kidneys

Cited by 16 publications

References 24 publications

Concentration of Myo-inositol in Skeletal Muscle of the Rat Occurs without Active Transport

Concentration of Myo-inositol in Skeletal Muscle of the Rat Occurs without Active Transport

Selective hormonal control of myo-inositol biosynthesis in reproductive organs and liver of the male rat.

Role of Parathyroid Hormone in the Decreased Motor Nerve Conduction Velocity of Chronic Renal Failure

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