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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Epinephrine-induced hyperglycemia was attenuated by the treatment of rats with pertussis vaccine, but this attenuation was abolished when endogenous insulin was suppressed by streptozotocin or anti-insulin serum. It was concluded that epinephrine-induced hyperglycemia was counterbalanced by the hypoglycemic action of insulin, the secretion of which was markedly potentiated in pertussis-sensitized rats. 2. Without epinephrine, no hypoglycemia developed in pertussis-sensitized rats despite the higher blood level of insulin. Tracer experiments with [14C,3H] glucose or [14C]bicarbaonate showed that, in pertussis-sensitized rats, more glucose was liberated into the blood from hepatic gluconeogenesis at the expense of hepatic glycogenesis, thereby accelerating the turnover of blood glucose. 3. Since this activation of hepatic glucose production was reduced by propranolol, a beta-adrenergic blocking agent, it is very likely that adrenergic beta-stimulation is, at least partly, responsible for the metabolic alterations observed in pertussis-sensitized rats.
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PMID:Accelerated turnover of blood glucose in pertussis-sensitized rats due to combined actions of endogenous insulin and adrenergic beta-stimulation. 12 60

Following the intravenous injection of streptozotocin into rats, postprandial hyperglycaemia was sustained from 24 hours over a subsequent period of some weeks and the rats were glucose intolerant. When streptozotocin was similarly injected into pertussis-sensitized or hydrocortisone treated rats, the postprandial hyperglycaemia observed at 24 hours did not persist, but showed a progressive decline until near normoglycaemia was obtained a week later. These animals manifested normal glucose tolerance one week after streptozotocin. Thus, a spontaneous recovery from streptozotocin-induced diabetes occurred under these conditions. This spontaneous recovery from diabetes was associated with hyperinsulinaemia in the fed state.
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PMID:Spontaneous recovery from streptozotocin-induced diabetes in rats pretreated with pertussis vaccine or hydrocortisone. 14 87

In order to study the mechanism by which pertussis-sensitized rats showed enhanced insulin secretory responses to various secretagogues (Sumi, T., and M. Ui, Endocrinology 97: 352, 1975), pancreases of rats receiving a single injection of Bordetella pertussis cells 3 days before were perfused with Krebs-Ringer solution, and release of insulin therefrom was compared with that from the pancreases of normal rats. Much more insulin was released from the pancreas of the pertussis-sensitized rat than from the pancreas of the normal rat in response to glucose, arginine, glibenclamide and 3-isobuty-l-methylxanthine. The inhibition of insulin secretion caused by epinephrine, norepinephrine or phenylephrine via alpha-adrenergic receptors in the pancreas of normal rats was no longer observable with the pancreas from pertussis-sensitized rats. Instead, the addition of epinephrine with or without phentolamine gave rise to a marked secretion of insulin from the pancreas of pertussis-sensitized rats which was prevented by propranolol. It is concluded that a single injection of B. pertussis into rats results in a sustained modification of insulin secretory processes in the pancreatic beta-cells in such a manner as to favor insulin secretory responses to beta-adrenergic stimulation and other secretagogues.
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PMID:Perfusion of the pancreas isolated from pertussis-sensitized rats: potentiation of insulin secretory responses due to beta-adrenergic stimulation. 19 99

The biological activities were studied of a new protein, islets-activating protein (IAP), purified from the culture medium of Bordetella pertussis. Rats injected intravenously with 1 microgram of purified IAP exhibited markedly enhanced insulin secretory responses to glucose, glucagon, epinephrine, and sulfonylureas over a period from 3 to 10 days after the injection. The degree and duration of the enhancement were proportional to the dose of IAP; the maximal effect induced by 1-2 microgram of IAP persisted for as long as 2 months. There was a highly significant correlation between the enhancement of insulin secretion and suppression of epinephrine hyperglycemia over a wide range of doses of IAP, indicating that suppression of epinephrine hyperglycemia resulted from hypoglycemic action of insulin secreted in response to epinephrine challenge. Additional actions of IAP were observed in mice; mice treated with higher doses of IAP showed symptoms were observed when lower doses of IAP were injected into mice. Thus, it is concluded that IAP is a protein primarily possessing a unique action to potentiate insulin secretory responses of experimental animals to nutritional and hormonal stimuli.
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PMID:Biological properties of islets-activating protein (IAP) purified from the culture medium of Bordetella pertussis. 20 75

The mechanism whereby "islet-activating protein" (IAP) purified from the culture medium of Bordetella pertussis potentiates insulin secretion was studied by experiments in vitro with islets of rats once injected with IAP (0.5 micrograms/100 g body weight, 3 days before killing) or with islets that had been exposed to IAP (0.1 to 100 ng/ml) for 24 h. The IAP treatment markedly enhanced insulin secretory responses and cAMP accumulation in islets, facilitated the efflux of 45Ca through the cell membrane, and abolished the alpha-adrenergic action of epinephrine (and somatostatin) to inhibit glucose-induced insulin release, cAMP accumulation, and 45Ca uptake. These effects of the IAP treatment were reduced when islets were incubated in a low calcium medium. Based on these results, it was concluded that IAP interacts directly but slowly with the islet B cell in such a manner as to render more calcium available to the stimulus-secretion coupling mechanism as a result of sustained activation of native calcium ionophores on the cell membrane.
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PMID:Islet-activating protein. Enhanced insulin secretion and cyclic AMP accumulation in pancreatic islets due to activation of native calcium ionophores. 21 76

The early phase of insulin secretion to an oral glucose load was blunted in spontaneous diabetic rats. The blunted insulin secretion was associated with markedly impaired glucose tolerance. A single injection of the islet activating protein (IAP), a protein derived from the culture medium of Bordetella pertussis, into the spontaneous diabetic rats normalised glucose tolerance. The increase in insulin response to glucose was an important contributing factor to the improvement of glucose tolerance. This curative effect of the IAP on the diabetic state was of long duration; glucose tolerance remained virtually normal over a period of one month in the diabetic rats. Perfusion of the isolated pancreas of the diabetic rats pretreated with IAP showed an increase in insulin response to glucose and loss of suppression of glucagon secretion by noradrenaline.
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PMID:Islet activating protein (IAP) derived from the culture supernatant fluid of Bordetella pertussis: effect on spontaneous diabetic rats. 34 42

Rats were injected once iv with an islet-activating protein (IAP), a new protein purified from the culture medium of Bordetella pertussis. Three days later, their pancreases were studied in vitro for insulin secretory responses. As with pertussis vaccine, pretreatment of rats with IAP was effective in enhancing insulin release from pancreas during perfusion or from islets during incubation in response to secretagogues such as glucose and glibenclamide. The alpha-adrenergic inhibition of insulin secretion induced by epinephrine was also reversed by the pretreatment with IAP. 3-Isobutyl-1-methylxanthine caused insulin release due to accumulation of cAMP. This 3-isobutyl-1-methylxanthine-induced insulin release during perfusion was enhanced in a Ca-containing perfusate, but was conversely reduced in a Ca-free perfusate by the IAP pretreatment. Upon the addition of Ca to the Ca-free perfusate, more insulin was released from pancreases of IAP-treated rats than from those of nontreated rats.
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PMID:Effect of in vivo pretreatment of rats with a new protein purified from Bordetella pertussis on in vitro secretion of insulin: role of calcium. 37 93

Humoral immunity to bacterial antigens was investigated in 68 tissue typed and glucose tolerance tested first degree blood relatives of insulin dependent diabetics (IDD). The data were compared with those obtained in 60 IDDs and in 55 healthy controls. The prevalence of bacterial antibodies to E. coli, staphylococci, pertussis and diphtheria toxins were just slightly, but not significantly reduced in the blood relations compared with controls. Incidence of antibacterial antibodies was almost identical in blood relations with impaired and in those with normal glucose tolerance. By contrast, antibody formation to E. coli and staphylococci (p less than 0,0005, p less than 0,0005) respectively was significantly impaired in IDD. No correlation between genes of the major histocompatibility complex and humoral antibacterial immunity could be observed in IDD and blood relations. In conclusion, antibacterial antibody formation was found to be severely impaired in IDD patients but to be almost normal in blood relations of insulin dependent diabetics. These findings suggest that the humoral antibacterial immunodeficiency observed in IDD is a disease associated process probably independent of major histocompatibility complex linked genes.
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PMID:Humoral antibacterial immunity in first degree relatives of insulin-dependent diabetics. 71 Jun 77

The increase in blood insulin level induced by adrenergic beta-stimulants, glucose and tolbutamide was strongly exaggerated in pertussis-sensitized rats. Moreover, the decrease in blood insulin caused by the alpha-receptor-mediated action of epinephrine in glucose- or tolbutamide-treated rats was effectively reversed by pertussis sensitization. The rise of blood insulin concentration due to adrenergic alpha-blockade was also enhanced by pertussis sensitization. It is concluded that the secretion of insulin resulting from the stimulation of adrenergic bate-receptor is enhanced by pertussis sensitization, probably due to activation of a process occurring in the chain of events leading to the discharge of insulin from the pancreatic beta-cell.
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PMID:Potentiation of the adrenergic beta-receptor-mediated insulin secretion in pertussis-sensitized rats. 115 56

The hypoglycemic effect of Bordetella pertussis (Challenge strain No.18323) purified cell extract (protein with traces of carbohydrates, 2 mg%) administered (0.1 mg/100 g body wt. i.v.) into mice on the activities of the key regulatory enzymes, viz. glucokinase, phosphofructokinase, pyruvate kinase, glyceraldehyde phosphodehydrogenase, glucose-6-phosphate dehydrogenase (G-6-PD) and lactate dehydrogenase, of glycolytic pathway in liver has been studied at varying intervals after injection. The maximum hypoglycaemic effect was observed at the end of 12 hr, while activities of all the enzymes studied showed significant enhancement after 18 hr, thus suggesting increased glucose utilization towards the formation of pyruvate. Actinomycin D is found to inhibit stimulation of G-6-PD activity in B. pertussis treated animals, thereby indicating the role of B. pertussis in synthesis of this enzyme.
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PMID:Bordetella pertussis extract induces increase in the activities of glycolytic enzymes in mouse liver. 128 37


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