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| 2. |
- Eriksson, Jan W, et al.
(författare)
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Vanadate increases cell surface insulin binding and improves insulin sensitivity in both normal and insulin-resistant rat adipocytes
- 1992
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Ingår i: Diabetologia. - 0012-186X .- 1432-0428. ; 35:6, s. 510-516
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was to elucidate the acute effects of vanadate on cell surface insulin binding and insulin sensitivity in rat adipocytes. The cells were preincubated at 37 degrees for 20 min followed by energy depletion with potassium cyanide, extensive washing and 125I-insulin binding. The presence of vanadate or insulin during the preincubation period dose-dependently enhanced 125I-insulin binding to normal adipocytes (maximally 4-5-fold) through an increased number of binding sites without any change in receptor affinity. Submaximal concentrations of vanadate added together with insulin enhanced the cellular sensitivity to the effect of insulin to stimulate 3-O-methylglucose transport. Vanadate, but not insulin, was also capable of increasing insulin binding as well as insulin sensitivity in insulin-resistant cells (treatment with N6-monobutyryl cAMP or amiloride and adipocytes from obese, aging rats). There was a correlation between the effect of vanadate to augment insulin binding and its ability to enhance cellular insulin sensitivity. Thus, the data suggest that short-term vanadate treatment improves insulin sensitivity through enhanced receptor binding and that this occurs in both normal and insulin-resistant cells.
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| 3. |
- Lönnroth, P, et al.
(författare)
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Peroxovanadate but not vanadate exerts insulin-like effects in human adipocytes
- 1993
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Ingår i: Diabetologia. - 0012-186X .- 1432-0428. ; 36:2, s. 113-116
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Tidskriftsartikel (refereegranskat)abstract
- Vanadate and peroxovanadate were recently reported to exert maximal or even supramaximal (peroxovanadate) insulin-like effects in rat adipocytes. To evaluate the response in human cells, isolated human adipocytes were exposed to insulin or various concentrations of vanadate (0-10 mmol/l) or peroxovanadate (0-5 mmol/l). Neither vanadate nor peroxovanadate affected 125I-insulin binding and insulin sensitivity. Vanadate exerted no apparent effect on 14C-U-glucose uptake, whereas 0.1 mmol/l peroxovanadate exerted a full insulin-like response (p < 0.001). No additive response was observed by combining either vanadate or peroxovanadate with insulin. Peroxovanadate at 0.1 mmol/l was as effective as insulin in inhibiting isoproterenol-stimulated lipolysis. Neither peroxovanadate nor insulin-inhibited lipolysis stimulated by N6-monobutyryl-cAMP, an analogue which is not hydrolysed by the cAMP-phosphodiesterase. It is concluded that peroxovanadate, but not vanadate, elicits a full insulin-like response in human adipocytes.
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| 4. |
- Tallroth, G, et al.
(författare)
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Neurophysiological changes during insulin-induced hypoglycaemia and in the recovery period following glucose infusion in type 1 (insulin-dependent) diabetes mellitus and in normal man
- 1990
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Ingår i: Diabetologia. - 1432-0428. ; 33:5, s. 319-323
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Tidskriftsartikel (refereegranskat)abstract
- Hypoglycaemia (median venous blood glucose 1.8 mmol/l; range 1.6-2.3) was induced by an intravenous infusion of regular insulin in eight patients with Type 1 (insulin-dependent) diabetes mellitus (age 28.0 +/- 7.4 years; mean +/- SD, duration 15.5 +/- 5.1 years) and in 12 age-matched healthy male control subjects. Multi-channel frequency analysis of electroencephalogram (electrophysiologic brain mapping) and recording of P300 and somatosensory evoked potentials were performed before, during and immediately after the hypoglycaemic period. The hypoglycaemia produced a significant increase in low frequency electroencephalographic activity in both groups, most pronounced over anterior regions of the brain. The electroencephalographic activity was normalised immediately after the hypoglycaemic period. The patients with diabetes showed somewhat longer P300 latencies during the initial normoglycaemic examination. Hypoglycaemia caused a marked reduction of the P300 amplitude in both groups of subjects and the amplitude was not restored immediately after normalisation of blood glucose levels. The somatosensory cortical responses were not affected by hypoglycaemia. We conclude that hypoglycaemia results in impairment in cerebral function, as measured by neurophysiological techniques, which is not immediately normalised when blood glucose is restored to normal.
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| 5. |
- Tallroth, G, et al.
(författare)
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The influence of hypoglycaemia on regional cerebral blood flow and cerebral volume in type 1 (insulin-dependent) diabetes mellitus
- 1993
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Ingår i: Diabetologia. - 1432-0428. ; 36:6, s. 530-535
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Tidskriftsartikel (refereegranskat)abstract
- The effect of moderate hypoglycaemia (venous blood glucose 2.0 +/- 0.2 mmol/l; mean +/- SD) on regional cerebral blood flow and cerebral volume was studied in a group of ten right-handed patients with Type 1 (insulin-dependent) diabetes mellitus (age 26.0 +/- 2.4 years, duration 18.4 +/- 3.8 years) using an intravenous Xenon 133 single photon emission computed tomography technique. After 10 min of hypoglycaemia, global cerebral blood flow had increased to 55.8 +/- 4.5 ml.100 g-1.min-1 compared to the initial normoglycaemic flow of 49.5 +/- 3.7 ml.100 g-1.min-1 (p < 0.01). A further increase in global cerebral blood flow to 59.5 +/- 4.5 ml.100 g-1.min-1 (p < 0.05) occurred 15 min after normalization of the blood glucose level. The global cerebral blood flow change from before hypoglycaemia to after recovery was inversely related to the initial glucose level. No change in the relative distribution of the regional cerebral blood flow was found between the measurements. The cerebral blood flow was significantly higher in the right hemisphere compared with the left hemisphere (2.3, 1.6 and 2.2%, respectively; p < 0.05) in all measurements. Deeper hypoglycemia was associated with a more pronounced decrease in brain volume, while the length of the restitution time after hypoglycaemia correlated with a volume increase. Due to influences with opposite effects there was no mean change in the brain volume.
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