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J Best

Publications and source records attributed to J Best.

At least 55 records · Page 3Linked to original sources

Insulin secretion, insulin sensitivity and glucose-mediated glucose disposal in thyrotoxicosis: a minimal model analysis.

In order to evaluate simultaneously in thyrotoxic subjects the relative contributions of insulin secretion, insulin-sensitivity (SI) and glucose-mediated (SG) glucose disposal to overall glucose tolerance, seven non-obese patients with thyrotoxicosis were studied by the minimal model analysis of the frequently sampled intravenous glucose tolerance test, before and greater than 1 month after being rendered euthyroid, and compared with eight healthy control subjects. Basal glucose, C-peptide and glucagon levels were similar in all groups but, in the toxic and euthyroid states, basal insulin levels were significantly elevated compared to the control group (11.2 +/- 2.0 and 7.9 +/- 1.1 vs 5.1 +/- 0.6 microU/ml, mean +/- SE, P less than 0.02). FFA levels were raised in the thyrotoxic subjects prior to treatment (0.95 +/- 0.11 vs 0.68 +/- 0.08 and 0.54 +/- 0.08 mmol/l, P less than 0.02). Glucose tolerance (Kg) was reduced in the thyrotoxic subjects compared to the euthyroid state (1.16 +/- 0.12 vs 1.44 +/- 0.13 per min, P less than 0.025) and control group (1.44 +/- 1.0 per min, 0.05 less than P less than 0.1). First phase (phi 1) and second phase (phi 2) insulin release were both significantly elevated in the thyrotoxic and euthyroid states compared to the control group (phi 1 7.10 +/- 1.88 and 5.29 +/- 1.03 vs 1.72 +/- 0.17 microU/mg/min X 10(-2), P less than 0.01; phi 2 18.64 +/- 3.14 and 16.74 +/- 4.48 vs 9.23 +/- 0.74 microU/mg/min X 10(-2) respectively, P less than 0.02). SG was similar in all groups but SI was significantly reduced in the thyrotoxic subjects compared to the control group (2.24 +/- 0.62 vs 5.92 +/- 1.50/min/microU/ml X 10(4), P less than 0.02) and rose post-treatment in the euthyroid subjects (4.23 +/- 1.75/min/microU/ml X 10(4)). In the thyrotoxic subjects before and after treatment, log SI correlated negatively with basal FFA levels (r = -0.57, P less than 0.05) and with phi 2 (r = -0.58, P less than 0.05). The fractional clearance rate of insulin was unaltered by the thyrotoxic state. It is concluded that in thyrotoxicosis the impairment of Kg is due to reduced insulin sensitivity in the presence of enhanced insulin secretion, but glucose-mediated glucose disposal is unaltered by the toxic state.

Adult↗

Ocular dominance plasticity in adult cat visual cortex after transplantation of cultured astrocytes.

During a critical restricted period of postnatal development, the visual cortical circuitry is susceptible to modifications that are dependent on experience. If vision is restricted to only one eye during this period, the territories innervated by the deprived eye shrink considerably, whereas those innervated by the non-deprived eye expand, and the deprived eye loses the ability to influence almost all of the cells in the cortex. Thus, changes in ocular dominance are paralleled and possibly mediated by synapse elimination and axonal sprouting. Hypotheses about the mechanisms underlying ocular-dominance plasticity assume the activation of NMDA (N-methyl-D-aspartate) receptors and subsequent calcium influx as a trigger of synaptic modifications. In addition, plasticity relies on functional neuromodulatory afferents. On the basis of immunocytochemical studies, it was recently proposed that the presence of immature astrocytes is a prerequisite for visual cortical plasticity, and that the end of the critical period is causally linked to the maturation of astrocytes. Here we report, in support of this hypothesis, that resupplementation of the visual cortex of adult cats with astrocytes cultured from the visual cortex of newborn kittens reinduces ocular-dominance plasticity in adult animals.

Animals↗