Biomedical subjects

F Q Nuttall

Publications and source records attributed to F Q Nuttall.

At least 145 records · Page 8Linked to original sources

PubMed1976

Phosphohistone and glycogen synthase D phosphatase activities in a liver glycogen pellet preparation.

A liver glycogen pellet preparation previously found to contain synthase D phosphatase activity was shown to contain also phosphohistone phosphatase activity. Pellet phosphohistone phosphatase and synthase D phosphatase competed for the same substrates and appeared to be the same enzyme. ATP, a potent inhibitor, and G-6-P, a potent activator of the synthase phosphatase reaction, had little effect on the phosphohistone phosphatase reaction. These observations suggest that the ATP and G-6-P effects are relatively specific and are probably caused by binding to the synthase D substrate. The observed effects of NaCl and KCl were more complex. They stimulated phosphohistone phosphatase activity but strikingly inhibited synthase phosphatase activity. Sodium fluoride inhibited both reactions.

Adenosine Triphosphate↗

PubMed1975

Characteristics of the dephosphorylated form of phosphorylase purified from rat liver and measurement of its activity in crude liver preparations.

The phosphorylated form of liver glycogen phosphorylase (alpha-1,4-glucan : orthophosphate alpha-glucosyl-transferase, EC 2.4.1.1) (phosphorylase a) is active and easily measured while the dephosphorylated form (phosphorylase b), in contrast to the muscle enzyme, has been reported to be essentially inactive even in the presence of AMP. We have purified both forms of phosphorylase from rat liver and studied the characteristics of each. Phosphorylase b activity can be measured with our assay conditions. The phosphorylase b we obtained was stimulated by high concentrations of sulfate, and was a substrate for muscle phosphorylase kinase whereas phosphorylase a was inhibited by sulfate, and was a substrate for liver phosphorylase phosphatase. Substrate binding to phosphorylase b was poor (KM glycogen = 2.5 mM, glucose-1-P = 250 mM) compared to phosphorylase a (KM glycogen = 1.8 mM, KM glucose-1-P = 0.7 mM). Liver phosphorylase b was active in the absence of AMP. However, AMP lowered the KM for glucose-1-P to 80 mM for purified phosphorylase b and to 60 mM for the enzyme in crude extract (Ka = 0.5 mM). Using appropriate substrate, buffer and AMP concentrations, assay conditions have been developed which allow determination of phosphorylase a and 90% of the phosphorylase b activity in liver extracts. Interconversion of the two forms can be demonstrated in vivo (under acute stimulation) and in vitro with little change in total activity. A decrease in total phosphorylase activity has been observed after prolonged starvation and in diabetes.

Adenosine Monophosphate↗

PubMed1975

Acute changes in thyroid function in patients treated with radioactive iodine.

Serum triiodothyronine (T3) and thyroxine (T4) were measured in thirteen unselected hyperthyroid patients before and at frequent intervals after iodine-131 treatment. There was an abrupt rise in T3 from a pretreatment mean of 250 ng/100 ml to a maximum of 365 ng/100 ml at 24 hours. Total T4 rose from a mean of 18.7 mug/100 ml to a maximum of 22.3 mug/100 ml at 24-48 hours. These findings may explain why an occasional patient develops acute thyroid crisis after radioiodine treatment.

Adult↗

PubMed1975

Insulin and epinephrine effects on heart glycogen synthase and phosphorylase activity.

The effect of intravenous epinephrine on heart glycogen synthase and phosphorylase systems in control and insulin-pretreated rats was studied. The percent of synthase in the I form decreased rapidly after epinephrine treatment but the change was small and sometimes not significant. In insulin-pretreated rats in which the percent synthase I was increased, epinephrine produced a definate and highly significant decrease. There was a simultaneous increase in percent phosphorylase a in both groups. The synthase and phosphorylase responses were statiscally significant at 2.5 mug epinephrine/kgor more. These data are compatible with a mechanism in which protein kinase is activated by an increased cAMP concentration and affects both the synthase and phosphorylasesystems simultaneously. Propranolol blocked the epinephrine effects on cAMP, synthase I, and phosphorylase a. Although insulin had little effect on the response ofthe synthase and phosphorylase systems to epinephrine, it nealry completely blocked glycogen degradation. The mechanism is unknown, but it appears to be due to an inhibition of phosphorylase a catalytic activity in vivo. Acetylcholine had no effect on synthase I, phosphorylase a, or cAMP in control or in insulin-pretreated animals.

Animals↗

PubMed1975

Calcium and folic acid absorption in patients taking anticonvulsant drugs.

Calcium and folic acid absorption were studied in 28 adult male epileptics on chronic anticonvulsant therapy. In 16 patients on diphenylhydantoin alone, calcium absorption was abnormal in 9. In 12 patients on both diphenylhydantoin and phenobarbital, calcium absorption was abnormal in 3 patients. Folic acid (3H-PGA) absorption was normal in all but one patient, while serum folate (less than 6.4 ng/ml) was reduced in all patients. Hypocalcemia (less than 8.5 mg/100 ml) occurred in only 2 patients, while serum alkaline phosphatase was elevated in 7 patients. These findings support the proposal that rickets and osteomalacia reported in patients on chronic anticonvulsant therapy results from reduced calcium absorption. The effect of these drugs appears to be the acceleration of the metabolism of vitamin D and an increase in the excretion of polar metabolites. This may result in reduced levels of 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol which are necessary for normal absorption of calcium. Since calcium absorption may be impaired secondary to a relative vitamin D deficiency, a supplemental increase in vitamin D intake by patients on anticonvulsant drugs is recommended.

Adult↗

PubMed1975

Familial hypokalemic periodic paralysis in blacks.

Two cases of familial hypokalemic periodic paralysis in Negro brothers occurred, and--because this has been reported to be an unusual disease among blacks--the family pedigree was investigated. Histories were obtained on 79 family members in four generations. Twenty seven (34%) had symptoms of periodic paralysis or weakness. As far as we could determine, there were no Caucasian ancestors.

Adult↗

PubMed1975

Thyroid function after radiation and surgery for head and neck cancer.

Preoperative radiation followed by surgical excision is accepted therapy for head and neck cancer. The effects of these modalities on thyroid function were evaluated in a prospective study. Sixty-one patients were given cobalt 60 radiation. Results showed that 41 patients (67%) were euthyroid, 12 patients (20%) were clinically and chemically hypothyroid, and 8 patients (13%) had transient loss of thyroid reserve. Permanent hypothyroidism occurred frequently in patients with hemithyroidectomy, but rarely in those treated with radiation alone. Onset of hypothyroidism was zero to six months, with transient loss of thyroid reserve occurring up to 18 months. This constitutes the initial report of an ongoing systematic study of thyroid function in such patients. The high incidence of hypothyroidism indicates a need for careful periodic evaluation.

Aged↗

PubMed1974