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Biomedical subjects

P Raskin

Publications and source records attributed to P Raskin.

At least 127 records · Page 7Linked to original sources
PubMed1978

Hyperglucagonemia and its suppression. Importance in the metabolic control of diabetes.

The role of glucagon in diabetes was studied in four patients with juvenile-type diabetes during continuous insulin infusion and a diet containing 150 g per day of carbohydrate. During insulin alone, plasma glucagon, measured at two-hour intervals, averaged 182 +/- 34 pg per milliliter, glucose 269 +/- 11 mg per deciliter, glucose excretion 52 +/- 8 g per 24 hours, ketone excretion 1.3 +/- 0.3 mmol per 24 hours, and urea nitrogen 12 +/- 2 g per 24 hours (mean +/- S.E.M.). Somatostatin (2 mg per day) lowered glucagon to 60 +/- 13 pg per milliliter, glucose to 111 +/- 17 mg per deciliter, glucose excretion to 1 +/- 0.7 g per 24 hours, ketone excretion to 0.5 +/- 0.2 mmol per 24 hours and urea nitrogen excretion to 8 +/- 2 g per 24 hours. Replacement of glucagon raised glucagon to 272 +/- 30 pg per milliliter, glucose to 202 +/- 20 mg per deciliter, glucose excretion to 14 +/- 7 g per 24 hours, ketone excretion to 0.8 mmol per 24 hours and urea nitrogen excretion to 11 +/- 2 g per 24 hours. In a subsequent study, similar improvement occurred on a diet of 30 g of carbohydrate daily, when absorption of dietary glucose was negligible. Hyperglucagonemia has an important role in diabetes; its correction reduces diabetic abnormalities to or toward normal.

Adult↗
PubMed1978

Diabetic regulation and its relationship to microangiopathy.

This review addresses the question of the effectiveness of rigid regulation of the blood glucose in delaying or preventing the vascular complications of diabetes mellitus. Morphometric, pathologic, biochemical, and clinical evidence on both sides of this question are presented. It is concluded that because of present inadequate methods of completely returning glucose homeostasis to normal in diabetics, the question remains moot.

Adult↗
PubMed1978

Glucagon and diabetes.

We have considered the evidence, first, that the presence of glucagon is essential in the pathogenesis of the full syndrome that results from complete insulin deficiency; second, that in the diabetic in whom insulin levels are relatively fixed, a rise in glucagon concentration contributes to endogenous hyperglycemia; and, third, that conventional methods of treatment of diabetes do not fully correct either the abnormal glucagon levels or the hyperglycemia, but when insulin therapy is supplemented with somatostatin, an agent which suppresses both glucagon and growth hormone, both hyperglycemia and hyperglucagonemia are corrected. These facts may one day provide a rationale for therapeutic efforts to suppress excess glucagon secretion in the management of diabetes in man.

Animals↗
PubMed1978

The hypercalciuria of diabetes mellitus: its amelioration with insulin.

Calcium and phosphous metabolism was investigated in 20 patients with diabetes mellitus when their diabetes was under poor metabolic control and again once optimal glycaemic control was achieved with aggressive insulin therapy. Ten of the twenty uncontrolled diabetics had hypercalciuria; insulin therapy returned calcium excretion to normal in five. Twenty-four hour calcium excretion fell in all but two patients when optimal diabetic control was achieved and calcium excretion was positively correlated with glucose excretion. Urinary cyclic AMP excretion, which was in the high normal range during poor control, decreased significantly during optimal insulin therapy. These data suggest that the hypercalciuria of uncontrolled diabetes may be a form of renal hypercalciuria which could result in parathyroid stimulation which might contribute to the development of osteopenia in patients with diabetes mellitus.

Adult↗
PubMed1978

Effect of streptozotocin-induced diabetes on hepatic ornithine decarboxylase activity in the rat.

The effect of diabetes on rat hepatic ornithine decarboxylase (ODC) activity was studied in male rats 4 h to 8 days after the ip or iv administration of streptozotocin. Hepatic ODC activity increased 4-fold above control on the fourth day of diabetes. Increased ODC activity was observed with a dose of streptozotocin (70 mg/kg iv) which increased plasma ketones and glucagon and reduced plasma insulin. No change was seen with doses causing only mild hyperglycemia without change in plasma ketones, glucagon, or insulin. Insulin therapy prevented the increase in hepatic ODC activity in diabetic rats. Adrenalectomy or hypophysectomy also prevented the diabetes-associated increase of ODC activity. The studies suggest that insulin deficiency may result in increased hepatic polyamine synthesis.

Adrenalectomy↗
PubMed1976

Effect of insulin on the exaggerated glucagon response to arginine stimulation in diabetes mellitus.

The effect of insulin on the glucagon response to intravenous arginine was studied in eight juvenile-type and six adult-onset diabetics. In the juvenile-type diabetics, concomitant administration of insulin significantly blunted the glucagon response from a mean maximal rise of 310 +/- 54 pg./ml. to only 184 +/- 39 pg./ml. (p less than 0.01), about the same as in nondiabetics. In the adult-onset patients, however, insulin had no effect, the mean maximal rise being 250 +/- 50 pg./ml. without insulin and 307 +/- 71 pg./ml. with insulin (N.S.). This study demonstrates that in juvenile-type diabetics concomitant administration of supraphysiologic quantities of insulin can reduce the exaggerated glucagon response to intravenous arginine to normal, whereas in the adult-type group, it has no apparent effect.

Adolescent↗
PubMed1975

Capillary basement membrane width in diabetic children.

The effect of juvenile onset diabetes mellitus on quadriceps muscle capillary basement membrane (QCBM) width has been examined by the electron microscopic morphometric method previously developed in this laboratory. The results demonstrate that in this age group QCBM thickening is strongly related to the age of the diabetic subject. As a result, in contrast to the almost constant thickening of QCBM that has consistently been documented in diabetic adults, QCBM hypertrophy is present in only 40 per cent of children with diabetes mellitus. As was previously shown to be the case in adults, in children, too, QCBM thickening is unrelated to the duration of the diabetes. Finally, the finding that QCBM hypertrophy is present at the time of acute onset of juvenile diabetes mellitus in 30 per cent of children, coupled with the fact that this lesion is not affected by duration of hyperglycemia, strongly supports our previous conclusion that diabetic microangiopathy is independent of the hyperglycemia of this disease. On the other hand, barring the possibility that microangiopathy in the pancreas precedes that in muscle, these results represent evidence against the suggestion that basement membrane hypertrophy represents the primary lesion of the diabetic syndrome.

Adolescent↗
PubMed1975

Effect of insulin-glucose infusions on plasma glucagon levels in fasting diabetics and nondiabetics.

The effect of the intravenous infusion of insulin plus glucose on plasma glucagon levels was studied in hyperglycemic fasting adult-type and juvenile-type diabetics and compared with fasting nondiabetics. Adult-type diabetics were given insulin for 2 h at a rate of 0.03 U/kg-min, raising their mean insulin to between 25 and 36 muU/ml; glucagon declined from a base-line value of 71+/-2 (SEM) to 56+/-1 pg/ml at 120 min (P less than 0.001). In juvenile-type diabetics given the same insulin-glucose infusion, glucagon declined from a base-line level of 74+/-8 to 55+/-5 pg/ml at 120 min (P less than 0.05). The absolute glucagon values in the diabetic groups did not differ significantly at any point from the mean glucagon levels in nondiabetics given insulin at the same rate plus enough glucose to maintain normoglycemia. When glucagon was expressed as percent of baseline, however, the normoglycemic nondiabetics exhibited significantly lower values than adult-type diabetics at 90 and 120 min and juvenile-type diabetics at 60 min. In nondiabetics given insulin plus glucose at a rate that caused hyperglycemia averaging between 134 and 160 mg/dl, glucagon fell to 41+/-7 pg/ml at 120 min, significantly below the adult diabetics at 90 and 120 min (P less than 0.01 and less than 0.05) and the juvenile group at 60 min (P less than 0.01). The mean minimal level of 39+/-2 pg/ml was significantly below the adult (P less than 0.001) and juvenile groups (P less than 0.05). When insulin was infused in the diabetic groups at a rate of 0.4 U/kg-min together with glucose, raising mean plasma insulin to between 300 and 600 muU/ml, differences from the hyperglycemic nondiabetics were no longer statistically significant. It is concluded that, contrary to the previously reported lack of insulin effect in diabetics during carbohydrate meals, intravenous administration for 2 h of physiologic amounts of insulin plus glucose is accompanied in unfed diabetics by a substantial decline in plasma glucagon. These levels are significantly above hyperglycemic nondiabetics at certain points but differ from normoglycemic nondiabetics only when expressed as percent of the baseline. At a supraphysiologic rate of insulin infusion in diabetics, these differences disappear.

Adolescent↗