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

The tendency of the pregnant diabetic to fasting ketosis limits the extent to which calorie restriction (particularly negative calorie balance) can be used in the treatment of the obese, adult-onset, pregnant diabetic. In addition, the vagaries of measuring excess weight gain and detecting extraneous sources of weight gain in diabetic pregnancy, and the difficulty of accurately enforcing a caloric prescription without forcing the subject to weigh her food, make the determination of an accurate degree of caloric limitation difficult at best. A greater reliance on the mother's appetite center may be more accurate and rewarding in most instances than any devices available to the clinician. Important considerations in the diet of the pregnant diabetic are adequate protein, minerals, and vitamins, an amount of carbohydrate that is constant from day to day but not necessarily restricted, carbohydrate intake in an unrefined form that maximizes the intake of associated fiber, and a reproducible meal and snack schedule which complements in insulin regimen. Insulin must remain the primary therapeutic tool if the effects of maternal diabetes on fetal morbidity and mortality are to be minimized.
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PMID:Dietary management of the pregnant diabetic. 39 66

Insulin dependent (IDD) and non-insulin dependent diabetes (NIDD) are separate disorders. Twin studies show that IDD cannot be entirely due to genetic causes as concordance is no more than about 50%, but there is some inherited predisposition to it as shown by HLA patterns. NIDD, on the other hand, is predominantly due to genetic causes since identical twins are nearly always concordant. Many cases of NIDD show chlorpropamide alcohol flushing (CPAF), a dominantly inherited feature which may precede the appearance of diabetes and thus act as a genetic marker for this type of diabetes. Diabetics who show chlorpropamide acohol flushing are less likely to develop retinopathy than those who do not. Genetic factors must therefore affect the incidence and severity of diabetic retinopathy. Chlorpropamide alcohol flushing is due to sensitivity to enkephalin. Enkephalin and other opioids affect carbohydrate metabolism and insulin release. It is possible therefore that they act as neurotransmitters and cause NIDD by a sympathetically mediated effect on the liver and pancreas--in other words, that as far as NIDD is concerned Claude Bernard's views on the cause of diabetes may have been right.
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PMID:Diabetes: the genetic connections. 39

In 55 poorly controlled insulin-dependent diabetics, we tried to discover criteria for an improvement of metabolism by means of the "artificial beta-cell" (Biostator). To this end, during the first 24 h of hospitalization, blood glucose was monitored continuously under conventional insulin therapy (monitoring period). Insulin requirement was determined during the next 24 h by the artificial beta-cell (feedback period). Corrections of diabetes regimen were made with reference to the insulin consumption during the feedback period and to the extent of the postprandial blood sugar increases and decreases during the monitoring period. The resulting new diabetes regimen led to a significant improvement of the daily blood sugar profiles.
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PMID:The artificial beta cell (Biostator) in the adjustment of instable diabetics--results after 20 months. 39 68

Insulin demand of 12 pregnant diabetics has been investigated with an artificial endocrine pancreas. A rise in insulin requirement during pregnancy which can be attributed to the effort of reaching normoglycemia and to the effect of contrainsular hormones has also been observed by this objective method. Assessment of basal insulin demand during the night might be helpful in optimizing conventional therapy by using long-acting insulins for supplementing basal insulin need. According to our results, pregnancy complicated by diabetes can be foreseen as one of the main applications of a glucose-controlled insulin infusion system.
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PMID:Use of an artificial endocrine pancreas in diabetic pregnancy. 39 75

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

In streptozotocin diabetes in the rat, growth hormone release-inhibitory hormone-like immunoreactivity (GHRIH-LI) content of pancreas, gastric antrum and colon was increased. Insulin therapy significantly lowered the increased pancreatic GHRIH-LI content but did not affect that of the gastric antrum and colon at the dosage used. The relevance of these findings in relation to pancreatic and gastrointestinal function in diabetes awaits clarification.
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PMID:Growth hormone release inhibitory hormone-like immunoreactivity in pancreas and gut in streptozotocin diabetes in the rat and response to insulin administration. 42 16

Administration of dichloroacetate (DCA) to normal rats resulted in a fall in serum glucose and triglycerides and a rise in ketone bodies. Insulin and cholesterol levels were unchanged. The effects of DCA on lipid metabolism were examined in isolated rat hepatocytes. At 10 mM DCA, the incorporation of tritiated water into fatty acids (saponifiable lipids) was inhibited by 33 +/- 4% (mean +/- SEM, N = 5). No effect on incorporation into cholesterol (measured as nonsaponifiable lipids) was observed. DCA inhibited the incorporation of 14C-glucose into lipid but had no effect on glucose oxidation. Fatty acid oxidation was increased by 76 +/- 7% (mean +/- SEM, N = 6). However, DCA had no effect on the recovery of newly synthesized lipid. Thus, inhibition of tritiated water incorporation into fatty acids represents decreased synthesis rather than increased turnover. DCA did not affect the incorporation of 14C-palmitate into triglycerides or phospholipids. Cell viability, as assessed by incorporation of 3H-isoleucine into protein and trypan blue exclusion, was not affected by DCA. These results suggest that DCA lowers serum triglycerides through inhibition of fatty acid synthesis and stimulation of fatty acid oxidation by liver.
Diabetes 1979 Apr
PMID:Effects of dichloroacetate on lipid metabolism in isolated rat liver cells. 43 64

In an attempt to determine whether the decreased number of insulin's receptors in obesity is a result of downregulation of the receptors, diazoxide (5 mg/kg/d) was given to 10 obese subjects. Insulin's suppression by diazoxide in these 10 subjects resulted in a mild glucose intolerance and an increase in insulin's receptors in seven of the 10 subjects. The subjects could be divided into three groups by analyzing the Scatchard plots of their insulin receptor studies before and after diazoxide. Four subjects exhibited an increase in both high affinity and low affinity receptors, three showed an increase only in high affinity receptors, and three failed to demonstrate any change in receptors in response to diazoxide. These studies support the concept that the decreased number of insulin's receptors observed in obesity is a result of the downregulation of the receptors and is not the primary, underlying cause of insulin resistance in obesity, although a contributory role cannot be ruled out.
Diabetes 1979 Apr
PMID:Downregulation of insulin receptors in obese man. 43 66

Insulin-degrading activity was measured in the 100,000g supernatant fraction of muscle, liver, and kidney from rats of varying ages. Young animals (four weeks old) had the highest activity in all three tissues. By seven weeks of age the activity in both muscle and liver had decreased significantly as compared with four-week-old animals. A slight but nonsignificant decrease occurred in kidney. In animals over one year of age the insulin-degrading activity in all three tissues was significantly less than the activities at either four or seven weeks. In contrast the effect of age on degradation of albumin and parathormone was much less marked.
Diabetes 1979 Apr
PMID:The effect of age on insulin-degrading activity in rat tissue. 43 72


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