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Biomedical subjects

S J Hurel

Publications and source records attributed to S J Hurel.

8 recordsLinked to original sources
PubMed1996

The short Synacthen and insulin stress tests in the assessment of the hypothalamic-pituitary-adrenal axis.

OBJECTIVE: The best dynamic test for the assessment of the hypothalamic-pituitary-adrenal axis and the interpretation of the cortisol levels, remain a matter of controversy. We aimed to establish normal ranges with current assays, for both the short Synacthen (SST) and insulin stress tests (IST) and then to use these data to examine whether the SST can satisfactorily substitute for the IST in assessment of the hypothalamic-pituitary-adrenal axis. DESIGN: Thirty SSTs and 27 ISTs were performed on different healthy volunteers. The results of all paired tests performed on patients in the last three years are reviewed. SETTING: Programmed Investigation Unit. SUBJECTS: Fifty-seven healthy volunteers and 166 patients. MAIN OUTCOME MEASURES: Basal serum cortisol concentration and cortisol values obtained at 30 and 60 minutes during the SST compared to the maximum obtained with adequate hypoglycemia (plasma glucose < 2 mmol/l) during an IST. RESULTS: From normal data the mean-2SD 30-minute value during the SST was 392 nmol/l and 60-minute value was 497 nmol/l. The maximal cortisol response (mean - 2SD) during the IST was 519 nmol/l. Sixty patients failed the IST, none of whom had a basal cortisol > 450 nmol/l and only six (10%) had a 30-minute cortisol value > 600 nmol/l. The 30-minute value provided a better index than the 60-minute value. The basal, 30 and 60-minute values during the SST all correlated positively and significantly with the maximal cortisol on IST. The correlations persisted for all microadenomas and macroadenomas secreting prolactin, gonadotrophins or growth hormone, patients undergoing either pre or post-adenomectomy evaluation, and in those patients who had received long-term steroids provided that the medication had been reduced and stopped two days prior to admission. CONCLUSIONS: Using a 30-minute cortisol value > 600 nmol/l as a cut-off, the short Synacthen test provides a suitable substitute for the insulin stress test. Adopting this policy will decrease the number of insulin stress tests performed by one-quarter and thus provide a substantial saving without detriment to patient care.

Adrenal Cortex Function Tests↗
PubMed1995

Inhibition of glycogen synthase kinase-3 by insulin in cultured human skeletal muscle myoblasts.

The acute effects of insulin on the activity of glycogen synthase kinase 3 (GSK-3) have been investigated both in the rat L6 muscle cell line and in cultured human myoblasts. The alpha and beta isoforms of GSK-3 are present in both cell types, with the beta isoform being predominant in the human cells. Insulin causes a rapid inactivation of both isoforms in both cell lines, with 50% inactivation being observed in the human myoblasts.

Amino Acid Sequence↗
PubMed1995

The effect of acute (60 minute) insulin stimulation upon human skeletal muscle glycogen synthase and protein phosphatase-1 in non-insulin-dependent diabetic patients and control subjects.

Previous studies have established that activation of muscle glycogen synthase (GS) is abnormal in non-insulin-dependent diabetes mellitus (NIDDM). Insulin-mediated activation of GS depends upon protein phosphatase-1 (PP1), which dephosphorylates the relevant sites of GS. In order to determine whether defects in PP1 activation cause subnormal activation of GS or whether PP1 activation itself is normal, we administered a short insulin infusion to 8 NIDDM subjects and 8 healthy controls matched for gender, age, and body mass index (BMI). GS fractional activity and PP1 activity were determined in biopsies taken from the gastrocnemius muscle before and after 60 min insulin infusion (0.1 U kg h-1). In the NIDDM group, muscle GS fractional activity was 6.8 +/- 1.6 and 10.0 +/- 1.5% (mean +/- SEM) (p = 0.11) before and after insulin infusion. In the control group, muscle GS fractional activity increased from 7.3 +/- 2.0 to 13.3 +/- 2.7% (p < 0.02). PP1 activity had returned towards basal levels after insulin infusion; NIDDM group 156 +/- 24.7 to 184.1 +/- 28.1 U mg-1; control group 220.8 +/- 30.1 to 233.8 +/- 29.8 U mg-1. In the NIDDM group there was a positive correlation between the increases in GS fractional activity and PP1 activity following insulin stimulation r = 0.77; p < 0.025). These data indicate that in vivo insulin-dependent activation of muscle PP1 is transient in normal subjects but is delayed in NIDDM. The defect in GS activation in NIDDM is likely to be proximal to PP1 in the pathway of transmission of the insulin signal.

Biopsy↗