Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether glucose intolerance in patients with chronic renal failure could improve by hemodialysis, the effects of arginine infusion on the concentration of blood sugar, insulin, glucagon, growth hormone were examined in healthy volunteers, undialyzed and dialyzed patients with chronic renal failure. Plasma concentrations of sugar and hormones in undialyzed and dialyzed patients responded similarly to arginine infusion. While blood samples were collected at 30, 45, 60, 90, 120 and 180 min after beginning infusion of arginine, the concentrations of sugar and hormones in both patients had no statistically significant differences. However, plasma concentrations of growth hormone in both patients 180 min after beginning of arginine infusion gave statistically significant differences. In the present study, the results suggest that hemodialysis might not improve the glucose tolerance in the patients with chronic renal failure.
Nephron 1979
PMID:Response of insulin, glucagon and growth hormone to arginine infusion in patients with chronic renal failure. 49 15

Effects of L-arginine (ARG) infusion on renal and systemic hemodynamics were studied in 12 anesthetized dogs. The experiment was performed in two groups of dogs. The dogs of group 1 (n = 6) received intravenous ARG at 2.5 mmol/kg followed by indomethacin (IND) injection (10 mg/kg) and were rechallenged with ARG at the same amount. The dogs of group 2 (n = 6) received intravenous ARG at 5 mmol/kg followed by IND injection (10 mg/kg) and were later infused with ARG at the same dose. In group 1, the first ARG infusion caused no significant changes in renal and systemic hemodynamics. During the second ARG infusion, glomerular filtration rate (GFR) and renal plasma flow (RPF) were significantly increased when compared with the IND-treated period. In group 2, the first ARG infusion increased cardiac output (CO) and decreased total peripheral resistance (TPR) without significant changes in GFR and RPF. The second ARG infusion induced acute rise of both GFR and RPF approximately twofold, compared with the IND-treated period. CO was also increased significantly. Plasma glucagon levels determined in 2 dogs showed an increase following both ARG infusions. These results indicate that an acute ARG loading induces renal and systemic vasodilatation in a dose-dependent manner despite IND effect, and would indicate that increased renal hemodynamics are not prostaglandin-mediated.
Nephron 1992
PMID:Effects of acute arginine loading on renal and systemic hemodynamics in dogs. 155 8

In 8 healthy normotensive probands with normal glomerular filtration rate, the effect of recombinant human growth hormone (rhGH) on inulin clearance (Cin) was examined in an open study with intraindividual crossover with or without enalapril pretreatment (20 mg/day). rhGH was administered by subcutaneous injection (4.5 U twice daly) for 3 days. On the following day Cin was measured with an enzymatic steady state infusion technique. Systemic hemodynamics and potential metabolic effects of rhGH, i.e., inulin-like growth factors I and II, somatomedin-binding protein, glucagon, C peptide, amino acid pattern, etc., were monitored. On controlled dietary intake of protein, the median Cin rose 72 h after start of rhGh administration from 114 (range 91-158) to 135 (108-167) ml/min/1.73 m2 without enalapril pretreatment (p less than 0.01) and from 111 (88-153) to 131 (100-173 ml/min/1.73 m2 with enalapril pretreatment (p less than 0.02). The results confirm that (1) rhGH increases Cin to a similar extent as extractive GH and (2) further demonstrate that this action is not obliterated by blocking the circulating converting enzyme.
Nephron 1990
PMID:Growth hormone induced rise in glomerular filtration rate is not obliterated by angiotensin-converting enzyme inhibitors. 169 55

In 24 patients with a kidney transplant and in 10 healthy subjects the test meal response of immunoreactive insulin (IRI), glucagon (IR-G), pancreatic polypeptide (IR-PP) and gastrin (IR-Ga) was studied. Patients with a kidney transplant showed significantly elevated basal plasma glucagon levels but normal levels of plasma IRI, IR-PP and IR-Ga. After administration of a test meal a significantly suppressed response of IRI, IR-PP and IR-Ga secretion was observed both in the patients treated with azathioprine as well as those treated with ciclosporin. In patients of the ciclosporin group the compromised response of IR-Ga and IRI secretion was significantly more marked than in subjects in the azathioprine group. From the results obtained in this paper it follows that the type of immunosuppressive drugs (azathioprine or ciclosporin) seems to be of minor importance in the pathogenesis of the described endocrine abnormalities.
Nephron 1990
PMID:Endocrine function of the pancreas and gastrin secretion in patients with a kidney transplant. 217 55

A 36-year-old man with ankylosing spondylitis, amyloidosis and chronic renal failure on maintenance hemodialysis developed severe hypoglycemia while being treated with propoxyphene. Upon discontinuation of the drug blood glucose levels returned to normal and hypoglycemia did not recur. Simultaneously with hypoglycemia, plasma glucagon and growth hormone levels were appropriately raised and serum insulin levels were adequately suppressed, thus ruling out hyperinsulinemia as the cause of hypoglycemia. A review of the literature disclosed four similar cases of propoxyphene-induced hypoglycemia, two of them with renal dysfunction. Propoxyphene should be remembered as a potential cause of hypoglycemia, particularly in patients with renal failure.
Nephron 1989
PMID:Propoxyphene-induced hypoglycemia in a patient with chronic renal failure. 279 48

Insulin induced hypoglycemia was produced in 5 chronic hemodialysis patients and 5 normal controls. Normally, several counterregulatory hormones (cortisol, growth hormone, glucagon and epinephrine) are secreted. Although we did not measure glucagon in our study, the other hormones were found to respond normally to the hypoglycemia in the control subjects. In the dialysis patients plasma epinephrine response was normal, but no responses of plasma ACTH, cortisol and growth hormone were found. Failure of the other counterregulatory hormones to respond to hypoglycemia indicates that dialysis patients probably maintain their euglycemic state by increasing plasma glucagon and epinephrine concentrations. We were unable to confirm the expected decrease of catecholamines that has been reported during hemodialysis.
Nephron 1988
PMID:Counterregulatory hormonal response to insulin-induced hypoglycemia in patients on chronic hemodialysis. 284 May 87

Treatment with thiazide diuretics causes an impairment of the glucose metabolism. To study whether this is due to a direct effect on the endocrine pancreas, the effects of the thiazide hydroflumethiazide on the release of glucagon, insulin, and somatostatin from the isolated perfused pancreas of normal and alloxan diabetic dogs were examined. Hydroflumethiazide at concentrations ranging from 1 to 50 micrograms/mL stimulated the normal secretion of glucagon (P less than 0.001), insulin (P less than 0.001), and somatostatin (P less than 0.001) in a dose-dependent manner. The normal hormone responses evoked by 50 micrograms/mL of the thiazide were, however, modified by the prevailing glucose level: higher insulin (P less than 0.05) and somatostatin (P less than 0.05) and lower glucagon (P less than 0.05) were obtained at the high glucose concentration of 11 mmol/L rather than at the low glucose concentration of 1.3 mmol/L. In alloxan diabetes, insulin secretion was almost extinct and did not respond to hydroflumethiazide, whereas glucagon was dose-dependently stimulated (P less than 0.001). In addition, we looked at the effect of the loop diuretic, bumetanide. The infusion of bumetanide at doses ranging from 0.5 to 3 micrograms/mL did not alter the release of glucagon, insulin, and somatostatin in the presence of 5.5 mmol/L glucose. The results suggest that hydroflumethiazide possesses the ability to directly stimulate A cell secretion in the normal and alloxan diabetic pancreas. Whether this effect is of clinical importance for the diminution in glucose tolerance observed during thiazide therapy remains, however, uncertain.
 ...
PMID:Effects of a thiazide diuretic (hydroflumethiazide) and a loop diuretic (bumetanide) on the endocrine pancreas: studies in vitro. 286 65

Uremia is associated with impairment of various cell-mediated immunity functions. The effect of parathyroid hormone (PTH) - known to be elevated in uremia - on several T cell functions has been studied. Normal peripheral blood lymphocytes incubated with increasing amounts of human PTH (HPTH) or bovine PTH (BPTH) showed a considerable decrease (up to 40%) in lectin-induced lymphocytes transformation, significant decrease in helpers to suppressors ratio, and marked inhibition of E rosette formation and T11-positive cells. PTH alone showed no cytotoxic effect on lymphocytes when incubated with or without mitogens. Glucagon, in concentrations up to 10-fold those found on uremia, had no effect on T cell function. Thus the effect of PTH was specific to the hormone action. The direct effect of PTH on normal T lymphocytes and some of their immunological responses is not clear. However, the results of this study support the hypothesis that excess blood levels of PTH may play a role in the pathogenesis of the impairment of the immune response in uremia.
Nephron 1988
PMID:In vitro effect of PTH on normal T cell functions. 297 21

Propranolol-induced hypoglycemia in hemodialysis patients has been increasingly recognized. We studied the effects of a nonselective beta-blocker (propranolol) and a beta 1-selective-blocker (metoprolol) on glucose metabolism during pharmacologic hyperglucagonemia in these patients. cAMP and insulin responses to glucagon were noted to be significantly higher in all patients after dialysis. This may possibly be due to the removal of a dialyzable factor suppressing these responses. However, despite a similar cAMP response, patients on propranolol had significantly lower glucose response than those not receiving beta-blocker before and after dialysis. While patients on metoprolol also had impaired glucose response before dialysis, this significantly improved after dialysis possibly due to the removal of active metabolite(s). Results suggest that metoprolol has less interference on glucose response to glucagon than propranolol in hemodialysis.
Nephron 1985
PMID:Effects of propranolol and metoprolol on glucose, cyclic AMP and insulin responses during pharmacologic hyperglucagonemia in hemodialysis patients. 298 50

Glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and humoral factors were simultaneously examined before and after a 50-gram oral protein load in 12 healthy controls and 12 nephrotic patients. The protein load led to rises in GFR with unchanged filtration fraction in both groups although the rate of increase in GFR was greater in the former. The levels of blood urea nitrogen, serum osmotic pressure, plasma glucagon and serum insulin, but not plasma angiotensin II, were significantly elevated following the protein load. The increase in GFR after the protein load appears to be mainly caused by increased ERPF and afferent arteriolar vasodilation.
Nephron 1988
PMID:Effects of an oral protein load on glomerular filtration rate in healthy controls and nephrotic patients. 334 49


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