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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

I.v. injection of 40 mg/kg or 65 mg/kg streptozotocin reliably induced diabetes in female Sprague-Dawley rats, but failed to induced hypertension within the following 42 days. In most animals injected with the higher dose and in some animals injected with the lower dose the tail blood flow was permanently impaired so that no blood pressure signals could be obtained by tail plethysmography. This phenomenon occurred also when the drug was injected into the jugular vein and thus was not due to a local effect of streptozotocin. 15 days after 65 mg/kg streptozotocin, the mean arterial pressure of the rats was similar to that of controls, when measured inthe awake state (carotid cannula) or under ether anaesthesia. 42 days after streptozotocin, under pentobarbital anaesthesia, the blood pressure was again normal in the animals given 40 mg/kg of the drug and depressed in the animals given 65 mg/kg of the drug 42 days previously. The increase of blood pressure induced by 1 microgram/kg (-)-noradrenaline i.v. was similar in the latter group of animals and in controls. The renal cortical renin concentration was much lower than in controls 42 days after either dose of streptozotocin, while the plasma renin activity was normal (40 mg/kg) or increased 65 mg/kg). The low renal renin content may have been due to the diabetic state, rather than to the drug itself. Adrenal medullary dopamine-beta-hydroxylase activity was increased 42 days after the higher dose of streptozotocin.
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PMID:Influence of streptozotocin-induced diabetes on blood pressure and on renin formation and release. 700 Dec 56

Insulin resistance was quantified with two different methods in 30 subjects with varying degrees of glucose tolerance. One method, the insulin suppression test, is performed by continuously infusing epinephrine, propranolol, insulin, and glucose. Epinephrine and propranolol suppress endogenous insulin release, and steady-state plasma levels of exogenous insulin and glucose are reached in all individuals. Because the steady-state insulin level is the same in all subjects, the height of the steady-state plasma glucose level provides a direct estimate of insulin resistance. The other method, the euglycemic clamp technique, produces a steady-state level of exogenous hyperinsulinemia by means of a primed and continuous insulin infusion. Glucose is also infused at a rate sufficient to prevent an insulin-induced fall in glucose concentration, and the amount of glucose required to maintain the basal plasma glucose level provides the estimates of insulin resistance. The results indicated that estimates of insulin resistance generated by the two methods were highly correlated (r = 0.93). Furthermore, both methods of assessing insulin resistance indicated that the greater the degree of glucose intolerance, the more severe the insulin resistance. These results serve to further emphasize the importance of insulin resistance in the pathogenesis of hyperglycemia in type II diabetes.
Diabetes 1981 May
PMID:Assessment of insulin resistance with the insulin suppression test and the euglycemic clamp. 701 7

Pressor responses to spinal sympathetic outflow and selected vasoactive agents were examined in control and diabetic Wistar-Kyoto pithed rats. Diabetes was induced by intravenous injection of alloxan (50 mg/kg). One week after the diabetogen, some of the rats were treated with one daily subcutaneous injection of Lente insulin (2 U/100 Gm) for five weeks. All rats were pithed at six weeks after alloxan. Vasoconstrictor responses to spinal sympathetic outflow, serotonin, norepinephrine, tyramine, and angiotensin were reduced in diabetic rats as compared to their age-matched controls. Administration of insulin caused only partial normalization of these responses. Nondiabetic rats given insulin exhibited vascular responsiveness similar to the treated diabetic group of animals. Blood pressures and heart rates were also found to be similar between the insulin-treated groups and significantly less than control. The finding that insulin does not produce complete normalization of vasoconstrictor responsiveness in diabetic rats may be relevant to the reduced blood pressure observed following insulin treatment.
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PMID:The effects of insulin on vasoconstrictor responses in pithed rats. 702 7

The control of glucose-6-phosphate dehydrogenase (G6PD) activity of the liver and brain were studied in normal and alloxan diabetic rats. Fasting decreased G6PD activity in brains and livers of normal rats significantly, but these decreases were reversed by placing the rats on a sucrose-rich diet. Injection of insulin were reversed by placing the rats on the sucrose-rich diet. Injection of insulin into normal 48h fasted rats had no significant effect on G6PD activity after 15 min. However, epinephrine significantly decreased liver G6PD activity by 17%, 7.5 min, after injection. Epinephrine had no effect on brain G6PD activity. In fed alloxan diabetic animals, the G6PD activity was found to be about 50% of that found in normal rats. Treatment of diabetic rats with protamine insulin partially reversed the decrease in G6PD activity caused by alloxan diabetes. It is concluded that insulin and epinephrine are important for the regulation of G6PD activity in vivo.
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PMID:The effects of alloxan diabetes, insulin and epinephrine on glucose-6-phosphate dehydrogenase from rat liver and brain. 702 49

To test the effects of acute cold on muscle amino acid and protein 1) rats were exposed to 4 degrees C for 24 h, functionally hepatectomized (eviscerated) and accumulation in the blood used to indicate changes in amino acid release from the tissues; 2) other rats were left intact, and urinary excretion of 3-methylhistidine (proportional to muscle protein breakdown) determined during cold exposure. In the eviscerated group, cold enhanced loss of total amino acids from the tissues (as alpha-amino nitrogen), but the loss (213 +/- 14.8% of basal in 2 h) was not due to excess alanine (180 +/- 8.5%). By comparison, in fasted rats total amino acid was 182 +/- 12.3, alanine 309 +/- 17.2%. Also, the cold-induced loss resembled the effects of streptozotocin diabetes and depended on a depression by cold of serum insulin (to 35.7 +/- 2.3 muU/ml). Therefore it was prevented when insulin was restored by infusion (40 mU . 100 g-1 . h-1) or by adrenodemedullation before cold exposure. Epinephrine (10 micrograms/100 g sc) depressed insulin in the latter and permitted amino acid release to recur. In intact rats, 3-methylhistidine excretion was unaffected by cold. The results suggest that although cold fails to stimulate alanine synthesis or protein breakdown, it inhibits insulin release sympathetically, thereby diminishing the amount of amino acid incorporated into muscle protein.
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PMID:Effects of acute cold exposure on muscle amino acid and protein in rats. 704 71

Stored sera from 466 patients with insulin-dependent diabetes mellitus and from 144 controls were examined for organ-specific antibodies to human adrenal cortex. Adrenal antibodies were found in seven of the patients with IDDM (1.5%) and in one control (0.7%). None of 91 black patients with IDDM had adrenal antibodies. All of the seven patients with adrenal antibodies had other organ-specific antibodies. Three had clinical hypothyroidism and one was thyrotoxic. All of these seven patients had a HLA-B8-bearing haplotype, suggesting that the B8-bearing haplotype confers an extremely high "relative risk" for adrenal autoimmunity in IDDM. Organ-specific autoimmune disease and/or organ-specific antibodies were found in 30% of the first-degree relatives of these eight probands with the adrenal antibodies (seven with IDDM and one control). We conclude that screening patients with IDDM for adrenal antibodies of low yield (1.9% among white patients). Further, adrenal antibodies may be present for at least two years without the development of Addison disease. Antibodies reactive only to the zona glomerulosa of the adrenal cortex may be benign. Patients with IDDM and thyroid microsomal antibodies are more likely to have adrenal antibodies (6.5%), as are patients with IDDM and a B8-bearing haplotype and those with IDDM and family histories of organ-specific autoimmunity.
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PMID:Adrenal autoantibodies and Addison disease in insulin-dependent diabetes mellitus. 740 Aug 84

Framingham Eye Study data were used to examine the effect of alternative definitions of open-angle glaucoma (OAG) on prevalence and on associations with selected variables from the Framingham Heart Study. Definitions were based on various combinations of history of glaucoma, types of visual field defects, and functions of intraocular pressure and cup-disc ratio. Visual field defect irrespective of blind spot enlargement is used as a standard for comparison. Prevalence of OAG by this definition is higher for men than for women and increases with age, more markedly than for most other definitions. Alcohol consumption is directly related to glaucoma defined either by the reference standard or by visual field defects including blind spot enlargement. Systemic blood pressure, ventricular rate, and diagnosis of diabetes are directly related to IOP.
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PMID:Alternative definitions of open-angle glaucoma. Effect on prevalence and associations in the Framingham eye study. 744 69

Plasma glucose concentration was measured at 3-h intervals in streptozotocin-induced diabetic rats placed on various insulin replacement regimens using three different kinds of insulin. High insulin dosages produced at least periodic hypoglycemia, even though there were no overt signs of insulin overdose. Low- and single-dose regimens produced periods of hyperglycemia. Both high and low doses of protamine zinc insulin normalized diabetes-induced reductions in 5-hydroxyindole-3-acetic acid [5-HIAA; the principal metabolite of 5-hydroxytryptamine (5-HT)] and 5-HT turnover (5-HIAA/5-HT), despite the failure of the low-dose regimen to normalize plasma glucose. Diabetic rats evidenced continued hyperphagia and hyperdipsia during insulin treatment, and insulin treatment also induced hyperphagia and excessive weight gain in nondiabetic rats. Insulin treatment only partially normalized diabetes-induced adrenal hypertrophy. Adrenal hypertrophy is an indication of a continued stresslike physiological state in diabetes even during insulin therapy. This state may be involved in the enhanced risk in diabetic humans for development of anxiety disorders and clinical depression.
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PMID:Metabolic and neurochemical profiles in insulin-treated diabetic rats. 750 9

Morphological analysis of hormone content and functional assessment of hormone secretion were conducted in beta TC-6 cells, an insulin-secreting cell line derived from transgenic mice expressing the large T-antigen of simian virus 40 (SV40) in pancreatic beta-cells. We observed by immunohistochemistry and confocal microscopy that beta TC-6 cells contain abundant insulin and small amounts of glucagon and somatostatin (SRIF). Glucagon usually co-localized with insulin, whereas cells containing SRIF did not contain insulin or glucagon. Static incubation and perifusion experiments demonstrated that beta TC-6 cells at passage 30-45 secrete insulin in response to glucose. In static incubations, maximal stimulation was achieved for glucose concentrations > 2.8 mmol/l glucose, and the half-maximal effect was observed at 0.5 mmol/l. Maximal stimulation was four times greater than HIT-T15 cells at passage 72-81, although HIT cells had a greater response over their basal levels. The magnitude of the insulin response to glucose in perifusion was 1,734 +/- 384 pmol.l-1. min and was 4.6-fold greater in the presence of 3-isobutyl-1-methylxanthine. Low amounts of glucagon were released in response to amino acids. Epinephrine (EPI), and to a lesser extent SRIF, inhibited phasic glucose-induced insulin secretion. A major portion of these inhibitory effects was mediated by pertussis toxin-sensitive substrates. Immunoblots detected the presence of the G-proteins Gi alpha 2, Gi alpha 3, and Go alpha 2. These results indicate that beta TC-6 cells are a glucose-responsive cell line in which insulin exocytosis is physiologically regulated by EPI and SRIF through Gi/Go-mediated mechanisms.
Diabetes 1995 Mar
PMID:Morphological and functional characterization of beta TC-6 cells--an insulin-secreting cell line derived from transgenic mice. 753 32

Gender differences in adrenal steroid hormone production and serum steroid hormone levels were compared in the spontaneous hypertensive/NIH-corpulent (cp) rat, which exhibits characteristics of both obesity and non-insulin-dependent diabetes mellitus. The study demonstrated that adrenal gland size correlated with adrenal production and serum levels of steroid hormones. Obese female SHR/N-cp rats were more steroidogenic than male SHR/N-cp rats; the size of their adrenal glands was twice that of the males (70 vs 33 mg). Body weights averaged 666 g for females and 829 g for males. Obese female rats had significantly higher serum concentrations of both corticosterone (827 vs 536 ng/ml) and aldosterone (675 vs 482 pg/ml) than obese male rats. As determined by in vitro assay, adrenal cortex production of corticosterone (2157 vs 1435 ng/30 min) and aldosterone (13.3 vs 9.5 ng/30 min) was significantly higher in obese female than in obese male rats. Adrenal production of testosterone in the in vitro assay was also significantly higher for obese female than male rats; however, adrenal estrogen production in obese rats did not differ significantly. The type of carbohydrate consumed (sucrose > starch) significantly affected serum levels of corticosterone, but not aldosterone, testosterone, or estrogen. Gender differences in adrenal steroid production and serum steroid levels suggest that hyperglycemia in obese SHR/N-cp rats may be, in part, the result of excess adrenal production of steroid hormones.
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PMID:Gender differences in adrenal cortex steroid production in SHR/N-corpulent rats. 780 Jun 80


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