Biomedical subjects

G M Bright

Publications and source records attributed to G M Bright.

25 records · Page 2Linked to original sources

PubMed1983

The effect of hyperglucagonaemia on blood glucose concentrations and on insulin requirements during fasting in insulin dependent diabetes mellitus.

The effect of sustained hyperglucagonaemia on blood glucose concentrations and on insulin requirements was evaluated in 6 fasting insulin dependent diabetic subjects whose blood glucose concentrations were being controlled with a closed loop insulin infusion system. Subjects were iv infused initially with either saline or glucagon and subsequently with the other infusate. All determinations were performed following the period during which transient increases in glucagon stimulated glucose production have been reported to occur. Plasma glucagon concentrations were significantly higher during the glucagon study period (491 +/- 65 vs 70 +/- 13 pg/ml +/- SD, P less than 0.001) as were blood glucose concentrations (104 +/- 2 vs 84 +/- 7 mg/ml +/- SD, P less than 0.001) and insulin requirements (3.5 to 36.5 vs 0 to 2.3 mU/kg/h, P less than 0.05). Sustained hyperglucagonaemia continues to have an effect on glucose homeostasis for at least 2 h following the initiation of a continuous infusion.

Adult↗

PubMed1983

Short stature associated with normal growth hormone and decreased somatomedin-C concentrations: response to exogenous growth hormone.

Two prepubertal males with low somatomedin-C concentrations in their sera, but normal growth hormone concentrations, had positive metabolic responses when human growth hormone was administered. An accelerated velocity of growth accompanied the long-term administration of growth hormone. This response was dependent upon the administration of exogenous hormone inasmuch as linear growth was subnormal both before and after administration of growth hormone. The extreme short stature in these individuals may be secondary to a biologically inactive growth hormone molecule that is immunologically reactive or to a decreased dose responsiveness of the cells that produce somatomedin when exposed to the usual concentrations of endogenous growth hormone.

Adolescent↗

PubMed1982

Organ-specific autoantibodies in children with common endocrine diseases.

Sera from 438 children were examined for autoantibodies to thyroid microsomes, thyroglobulin, pancreatic islet cells, gastric parietal cells, and adrenocortical cells by indirect hemagglutination and immunofluorescence techniques. A modification of the indirect hemagglutination technique allowed specific detection of low titers of antithyroidal antibodies. The subjects included a control group (117) with no known autoimmune disease, and children with disorders of the thyroid (88), insulin-dependent diabetes mellitus (201), Turner's Syndrome (24), and Addison disease (8). A subject's age at the time of disease onset and the race and sex were correlated with the prevalence of autoantibodies. The coincidence of autoantibodies to components of the thyroid with autoantibodies to gastric parietal cells was increased in children with disorders of the thyroid (94%, 18/19) over that observed in diabetes (29%, 4/14), Turner syndrome (0%), or Addison disease (0%), perhaps indicating different genetic propensities for the development of parietal cell antibodies in these groups. Islet cell antibodies were not found in subjects with Turner syndrome, nor were they more prevalent in white or black subjects with diabetes. The incidence of organ-specific autoantibodies in individuals without overt clinical disease may reflect an altered immunologic state that will lead eventually to autoimmune disease. Islet cell antibodies decline in prevalence in diabetes, whereas thyroid antibodies in disorders of the thyroid do not; this may reflect differences in the pathogenesis of these common autoimmune endocrine disorders in children.

Addison Disease↗

PubMed1980