| 1. |
- Agardh, Carl-David, et al.
(författare)
-
Urinary N-acetyl-beta-D-glucosaminidase activity does not predict development of diabetic nephropathy
- 1987
-
Ingår i: Diabetes Care. - : American Diabetes Association. - 1935-5548 .- 0149-5992. ; 10:5, s. 604-606
-
Tidskriftsartikel (refereegranskat)abstract
- Urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) has been suggested as a marker for diabetic nephropathy. In this study, urinary activity of NAG was measured with an interval of 5 yr in 36 insulin-dependent diabetic subjects to evaluate its predictive value for development of diabetic nephropathy. During the observation period, 9 patients developed detectable signs of diabetic nephropathy. In these patients, urinary albumin concentration had increased to 503 +/- 185 mg/L, compared to 16 +/- 1 mg/L in patients without nephropathy (P less than .01; means +/- SE), and the fractional albumin excretion rate was 0.21 +/- 0.07 X 10(-3), compared to 0.01 +/- 0.00 X 10(-3) (P less than .01). However, the activity of urinary NAG was not different in these patients compared with the patients without nephropathy (0.69 +/- 0.15 and 0.61 +/- 0.09 U/mmol creatinine, respectively). Furthermore, no increase in the activity of urinary NAG was seen during the observation period in either group. We concluded that the urinary activity of NAG is not related to the development of microalbuminuria and therefore cannot be used as a predictor for the development of diabetic nephropathy.
|
|
| 2. |
- Agardh, Elisabet, et al.
(författare)
-
Normal eyes in type 1 diabetics stay normal after one year of treatment with continuous subcutaneous insulin pump
- 1986
-
Ingår i: Acta Ophthalmologica. - 0001-639X. ; 64:5, s. 530-532
-
Tidskriftsartikel (refereegranskat)abstract
- Seven patients with type 1 diabetes mellitus were restored to near normoglycaemia by treatment with continuous subcutaneous insulin infusion pumps (CSII). The patients were examined with ophthalmoscopy, fundus photography and fluorescein angiography before and one year after the start of CSII treatment. In addition, ophthalmoscopy was performed after 6 months of treatment. All 14 eyes were normal prior to the CSII treatment and none had developed any signs of retinopathy after 6 months or 1 year. It is concluded that metabolic control can be near normalized with CSII treatment without any risk for development of diabetic microangiopathy in type 1 diabetics with normal eyes.
|
|
| 3. |
- Agardh, Elisabet, et al.
(författare)
-
Retinopathy and nephropathy in insulin-dependent diabetics: an inconsistent relationship?
- 1987
-
Ingår i: Diabetic Medicine. - 1464-5491. ; 4:3, s. 248-250
-
Tidskriftsartikel (refereegranskat)abstract
- The association between retinopathy and nephropathy was investigated in a retrospective study of 52 insulin-dependent diabetics with preproliferative or proliferative retinopathy and in 48 patients without or with background retinopathy. The duration of diabetes was 23.2 +/- 1.0 years (mean +/- SEM) and 22.0 +/- 1.2 years in the two groups. Patients in the retinopathy group showed a higher frequency of detectable nephropathy and were more often treated with antihypertensive drugs. However, a high proportion (35%) of patients with proliferative retinopathy did not show any detectable signs of nephropathy. Furthermore, nephropathy did not seem to develop in patients with retinopathy during an observation period of up to 9 years. The data suggest that the factors underlying the development of retinal and renal microangiopathy might be of different origin.
|
|
| 4. |
- Tallroth, G., et al.
(författare)
-
Neurophysiological changes during hypoglycaemia in type 1 (insulin- dependent) diabetes mellitus and in normal man
- 1990
-
Ingår i: Diabetologia. - 0012-186X .- 1432-0428. ; 33:5, s. 319-323
-
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.
|
|
| 5. |
- Tallroth, G, et al.
(författare)
-
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
-
Ingår i: Diabetologia. - 1432-0428. ; 33:5, s. 319-323
-
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.
|
|
| 6. |
- Tallroth, G, et al.
(författare)
-
Regional cerebral blood flow in normal man during insulin-induced hypoglycemia and in the recovery period following glucose infusion
- 1992
-
Ingår i: Metabolism, Clinical and Experimental. - : Elsevier BV. - 1532-8600. ; 41:7, s. 717-721
-
Tidskriftsartikel (refereegranskat)abstract
- The effect of moderate hypoglycemia (p-glucose, 2.0 +/- 0.3 mmol/L; mean +/- SD) on regional cerebral blood flow (rCBF) was studied in a group of 10 healthy, right-handed men (aged 23 to 28 years) using an intravenous xenon 133 single photon emission computed tomography technique (SPECT). After 10 minutes of hypoglycemia, global CBF had increased to 46.3 +/- 9.6 mL/100 g/min compared with the initial normoglycemic flow of 38.6 +/- 6.8 mL/100 g/min (P less than .01). The relative distribution of the rCBF changed significantly (P less than .05, ANOVA) from before to during hypoglycemia. Of the 10 regions analyzed, the highest increments in rCBF during hypoglycemia were found in the frontal (21.5% +/- 15.2%) and parietal (20.6% +/- 14.2%) lobes, and the lowest (10.7% +/- 9.4%) were found in the pons/brainstem regions. The increase in rCBF persisted for 15 minutes after normalization of blood glucose. The persisting high flow after hypoglycemia affected all regions, but a further 10.1% +/- 7.2% increase was observed in the pons/brainstem area (P less than .05). The CBF was significantly higher in the right compared with the left hemisphere (2.8%, 1.2%, and 3.9%, respectively; P less than .05) in all measurements. A decrease in brain volume was found at the final examination, compared with the hypoglycemic state (2.6%; P less than .05). It is concluded that moderate hypoglycemia leads to a marked increase in CBF and in the relative distribution of rCBF, which persists in the immediate period after normalization of the blood glucose level.
|
|
| 7. |
- Tallroth, G, et al.
(författare)
-
The influence of hypoglycaemia on regional cerebral blood flow and cerebral volume in type 1 (insulin-dependent) diabetes mellitus
- 1993
-
Ingår i: Diabetologia. - 1432-0428. ; 36:6, s. 530-535
-
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.
|
|
| 8. |
- Tallroth, G, et al.
(författare)
-
The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent) diabetes mellitus and in normal man
- 1992
-
Ingår i: Diabetes Research (Edinburgh, Scotland). - 0265-5985. ; 20:3, s. 73-85
-
Tidskriftsartikel (refereegranskat)abstract
- The changes in plasma gastrin-releasing peptide (GRP), arginine vasopressin (AVP), neuropeptide Y (NPY), corticotropin releasing hormone (CRH), galanin, ACTH, cortisol, delta sleep-inducing peptide (DSIP), adrenaline, noradrenaline and pancreatic polypeptide (PP) were measured after 5 and 15 minutes of acute insulin-induced moderate hypoglycaemia (2.0 mmol/l) in 10 patients with Type 1 diabetes mellitus with no autonomic neuropathy and in 10 healthy subjects. Plasma catecholamine and PP levels rose in both groups in response to hypoglycemia and the secretory response of ACTH was lower in the diabetic subjects (p < 0.01). GRP concentrations increased during hypoglycaemia (p < 0.01) while a reduction in AVP occurred at the start of hypoglycaemia (p < 0.001). The plasma AVP concentrations were higher in the diabetic group compared with those in the normal group (p < 0.05). The NPY concentrations were higher in the normal subjects (p < 0.05) but no change in the mean level occurred in either group during hypoglycaemia. No group differences or changes in mean plasma concentrations were found for galanin, DSIP and CRH. These observations support the view that regulatory peptides, if involved in glucose homeostasis, may rather have a modulatory effect than a direct action in restoring normoglycaemia.
|
|
| 9. |
- Wirsen, A, et al.
(författare)
-
Neuropsychological performance differs between type 1 diabetic and normal men during insulin-induced hypoglycaemia
- 1992
-
Ingår i: Diabetic Medicine. - 1464-5491. ; 9:2, s. 156-165
-
Tidskriftsartikel (refereegranskat)abstract
- Cerebral function was measured with a neuropsychological test battery before, during, and after insulin-induced hypoglycaemia (blood glucose approximately 2.0 mmol l-1) in 10 male Type 1 diabetic patients (age 20-43 years, duration of diabetes 14 (2-30) years) and in 12 normal men. There were no group differences in neuropsychological results at normal glucose levels. Significant effects of hypoglycaemia were found in reaction-time measures (p less than 0.001) and in other tests requiring speed and attention (p less than 0.001), in verbal fluency (p less than 0.05), and short-term memory (p less than 0.001). Significant group effects and interactions (p less than 0.05) revealed that the diabetic patients were generally more affected by hypoglycaemia than the normal subjects. This might have been partly due to the larger absolute decrease in blood glucose level in the diabetic patients, although the rate of glucose decrease was not related to performance in either group. Thus, the diabetic brain might be more vulnerable to hypoglycaemia, perhaps through the persistent impact of repeated hypoglycaemic episodes, although no neuropsychological deficit is demonstrable at normal blood glucose levels.
|
|
