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

A 53 year old woman presented with diabetes mellitus, hyperglucagonemia (600 to 1,500 pg/ml), clinical hyperparathyroidism and an abdominal mass diagnosed on biopsy as an islet cell carcinoma. Glucagon content of the tumor was 0.78 mug/g wet weight. Hourly blood samples during a 24 hour period revealed a direct correlation between plasma glucose and glucagon. The oral administration of glucose paradoxically increased whereas the intravenous administration decreased plasma glucagon. Circulating glucagon levels were markedly increased with arginine and epinephrine infusion. Both short- and long-term administration of alpha adrenergic blockade depressed the glucagon response to epinephrine infusion. In contrast, long-term alpha adrenergic blockade increased glucagon secretion despite improved glucose tolerance during a second 24 hour study. Although the patient demonstrated overt clinical and chemical findings of hyperparathyroidism, parathyroid hormone (PTH) was not detected in her plasma. The pattern of tumor growth was consistent with an origin from pancreatic islets. We conclude that (1) the tumor was responsive to physiologic stimuli known to affect glucagon secretion; (2) elevations of plasma glucagon levels with oral and dietary glucose suggest regulation of secretion by intestinal factors; and (3) improvement of glucose tolerance with alpha adrenergic blockade may be related to increased insulin secretion.
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PMID:Uncontrolled diabetes mellitus and hyperglucagonemia associated with an islet cell carcinoma. 4 4

Alteration of growth of dimethylbenz[a]anthracene-induced mammary tumors was caused by removal of estrogen (ovariectomy), or insulin (diabetes), or by inhibition of prolactin secretin (treatment with an ergoline derivative). The levels of cyclic AMP (cAMP) and cGMP were measured in carcinomas classified as growing, static, and regressing. The amount of cAMP, expressed as pmoles/mg tumor weight or pmoles/mg protein, was lowest in growing tumors, intermediate in static tumors, and highest in those regressing. No correlation was seen between tumor growth and cGMP levels. Cyclophosphamide-induced tumor stasis did not elevate cAMP levels. The data suggest a role of cAMP in arrest of hormone-induced tumor growth.
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PMID:Relationship of adenosine 3',5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate to growth of dimethylbenz(a)anthracene-induced mammary tumors in rats. 17 3

Specific iodine-125-labeled prolactin binding was measured in membrane particles prepared from R3230AC mammary carcinoma and liver of tumor-bearing Fischer rats after either prolactin, estrogen, or lergotrile mesylate treatment, or after the induction of diabetes by streptozotocin. Hormone binding to tumors was decreased by treatment with prolactin (.5 or 1 mg/day) or estradiol valerate (7.5 mg/kg/week). In contrast, prolactin treatment was without affect on prolactin binding to liver membrane particles, but estradiol valerate treatment resulted in a 4-fold increase in prolactin binding to this tissue. Lergotrile mesylate, which lowers plasma prolactin levels, had no affect on tumor growth or prolactin binding to either tumor or liver. Prolactin binding to both tumor and liver was significantly reduced in diabetic rats, suggesting that insulin may play an important role in controlling tissue sensitivity to prolactin. Specific binding of iodine-labeled prolactin to enzymatically dissociated cells from R3230AC tumors was demonstrated in vitro. The binding capacity of the cells was found to be of the same order of magnitude as the binding capacity in membrane preparations when appropriate corrections were applied for yields of cells and membranes. R3230AC tumor, which is responsive to prolactin, appears therefore to be a useful model system for further study aimed at elucidation of growth and metabolic response to the hormone prolactin in breast cancer.
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PMID:Prolactin binding to R3230AC mammary carcinoma and liver in hormone-treated and diabetic rats. 18 51

Growth rates of 7,12-dimethylbenz(a)anthracene-induced mammary tumors and the specific 125I-labeled prolactin binding to membrane fractions prepared from livers and tumors were studied in rats made diabetic by streptozotocin injection. Growth was inhibited in a majority of tumors and prolactin binding was reduced in both tumors and livers from diabetic animals. Prolactin binding to individual tumors varied over a wide range in both intact and diabetic animals. Scatchard analysis of binding data revealed that the apparent affinity of prolactin binding to liver and tumor membranes was similar (Ka approximately 3.0 X 10(9) M-1) and was not affected by diabetes. We suggest that the reduction in prolactin binding to tumors may render these tissues less responsive to prolactin and thereby explain, at least in part, the observed inhibition of tumor growth in diabetic rats. However, some tumors in diabetic animals regressed despite relatively high levels of prolactin binding activity. Therefore, additional factors most certainly play important roles in the mechanism(s) by which the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is impaired in the diabetic rat.
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PMID:Prolactin binding to 7,12-dimethylbenz(a)anthracene-induced mammary tumors and liver in diabetic rats. 40 90

Insulin and estrogen binding have been determined in 7,12-dimethylbenz(a)anthracene-induced mammary tumors of rats in various endocrine states. Hormonal therapy, such as diabetes and ovariectomy, resulted in differential effects on growth patterns and hormone binding of tumors coexisting in the same host or in different hosts. It was observed that tumors that continued to grow after the host was made diabetic (insulin independent) or started to regress after ovariectomy (ovarian dependent) demonstrated decreased insulin binding. Tumors that regressed in diabetic hosts (insulin dependent) or continued to grow in ovariectomized animals (ovarian independent) showed an increased insulin-binding capacity. No significant change in insulin binding was observed in tumors that remained static after ovariectomy or induction of diabetes. Estrogen binding in tumor cells from diabetic rats paralleled the pattern of tumor growth response to diabetes; insulin-independent tumors demonstrated a significant increase in binding compared to tumors from intact hosts, and insulin-dependent tumors showed decreased estrogen receptor levels. From these results, we conclude that (a) insulin plays a positive role in regulating estrogen-binding capacity, (b) ovarian hormones may play a role in regulating insulin-binding capacity, and (c) a relationship between insulin and ovarian hormones and the growth of 7,12-dimethylbenz(a)anthracene-induced tumors is strongly suggested and may have therapeutic implications.
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PMID:Relationship between insulin and estrogen binding to growth response in 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors. 41 34

Hypoglycemia and hypoinsulinemia accompanied i.p. or i.m. growth of the Ehrlich tumor in CBA/H and BALB/c mice. Simultaneously, insulin accumulated in the ascitic fluid of tumor-bearing mice. In hosts rendered diabetic by means of alloxan, the tumor decreased the blood glucose almost to the level seen in nondiabetic mice. Tumor growth was retarded in diabetic hosts, but cells from such tumors, transplanted into secondary diabetic recipients, grew faster than in their primary diabetic hosts, similarly to "nondiabetic" tumor cells growing in nondiabetic hosts. This phenomenon of "adaptation" of the tumor to the diabetic state was prevented if diabetic tumor-bearing mice were daily treated with insulin. The tumor did not grow in all diabetic recipients; the frequency of takes correlated with severity of the diabetes, i.e., with the dose of alloxan given to induce it. The greater the dose, the less mice accepted the tumor. Insulin injection into diabetic tumor-bearing mice promoted the tumor growth. Simultaneous treatment of diabetes and the tumor afforded the best antitumor effect.
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PMID:Growth and treatment of Ehrlich tumor in mice with alloxan-induced diabetes. 42 13

Methylcholanthrene-induced sarcomas (MCA-S) have different growth patterns in diabetic (D) and nondiabetic (ND) rats. Diabetes delays the early phase of tumor growth and prolongs survival. This study evaluated MCA-S growth and its relation to insulin receptors (IR) and glucose uptake. Fisher 344 rats 150-200 g were assigned to two groups: Diabetic tumor bearers (DTB, n = 26) and nondiabetic tumor bearers (NDTB, n = 18). Diabetes was induced with iv streptozocin (40 mg/kg); MCA-S was inoculated (1 X 10(6) cells) subcutaneously 10 days later. Animals were sacrificed during early growth (tumor volume less than or equal to 20 cc) or logarithmic growth (tumor volume greater than 20 cc). IR assay was performed (0-10(5) ng/ml cold insulin, 25 X 10(3) cpm/tube A14 125I-insulin, 90 min, 15 degrees C, pH 7.8) on a single cell preparation. Serum glucose milligrams per deciliter and insulin nanograms per milliliter were assayed. Glucose uptake (dpm/g tissue/hr) was assayed 2 hr after an ip injection of 0.5 microCi 3-O[14C]methylglucose. Diabetic, tumor-bearing animals had a significantly increased number of insulin receptors at the small [less than or equal to 20 cc, 28.7 (D) vs 8.3 (ND)] and large [greater than 20 cc, 82.8 (D) vs 27.8 (ND)] tumor volumes. Glucose uptake was increased in the tumor at both volumes in the non-diabetic animals compared to the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in insulin receptors on methylcholanthrene-induced sarcoma during growth. 219 Nov 69

Although there is a broad consensus on diabetes as a factor frequently associated with breast cancer its causal role has not been proved yet. Some pathophysiological mechanisms and pathways are well investigated (e.g. insulin acts as a growth factor or certain interrelations between endocrine regulation, tumor growth, and differentiation) but important questions remain unsolved like the influence of an altered glucose metabolism on tumor growth or to what extent risk factors for breast cancer interfere. A review is given about the experimental studies on insulin as a growth factor and its influence on the hormone receptors of the cancer cell as well as epidemiologic studies concerning the association between diabetes and breast cancer. Summarizing the results there is no clear evidence for determining diabetes mellitus as a risk factor for breast cancer. Further investigations are necessary for deriving conclusions relevant for cancer control measures.
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PMID:[The present state of knowledge on the problem of the relation between diabetes mellitus and breast cancer]. 268 78

Phosphatidylinositol (PI) kinase was characterized, its activity was measured in plasma membrane-enriched fractions of R3230AC rat mammary tumors, and these results were compared to enzyme activity in normal mammary glands at various stages of differentiation. PI kinase activity was found to be highest in mammary adenocarcinomas, whereas the mammary gland displayed the following order of decreasing activity: late lactation greater than early lactation greater than late pregnancy. Although diabetes only slightly increased tumor membrane PI kinase activity, insulin treatment of tumor-bearing diabetic rats, which reduced R3230AC tumor growth, caused a significant reduction (30 to 40%) in PI kinase activity. These results imply that PI kinase activity may be correlatable with normal mammary gland differentiation and with mammary tumor growth behavior. Formation of phosphatidylinositol-4-phosphate in tumor membranes was inhibited by low concentrations of calcium (microM range), suggesting the presence of calcium-sensitive polyphosphoinositide metabolism in the R3230AC carcinoma.
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PMID:Membrane-associated phosphatidylinositol kinase of R3230AC mammary tumors and normal mammary glands and effects of insulin on tumor enzyme activity. 284 58

Epidemiological data from different populations have suggested positive relationships between the incidence of colon cancer and meat and fat intake and a negative relationship with dietary fiber consumption. Within population comparisons have been less clearcut. Current theories on colonic carcinogenesis in man involve increased concentrations of bile acids and their metabolites, alterations in colonic pH, low Ca++, raised NH3 and long chain fatty acid levels, and alterations in bacterial numbers, type, and metabolic capabilities. The many laboratory studies in rats have been difficult to interpret since powerful initiators of carcinogenesis are always required and this rather than the promotion of spontaneous neoplastic change is the sine qua non for tumor growth in this situation. The current dilemma highlights the lack of knowledge of most aspects of human colonic physiology. Until these issues are more clearly resolved the epidemiological leads would point to low fat diets rich in less processed starchy foods with increased fiber as possible protection. Such advice is in common with the pronouncements of heart foundations, diabetes associations, and recommendations of official bodies to the general public.
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PMID:Cancer risk: possible protective role of high carbohydrate high fiber diets. 302 Sep 71


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