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

The effect of normal and gestational-diabetic pregnancy on the gastroenteropancreatic (GEP) hormone response to lipid ingestion was studied in 17 women, 8 normal and 9 with gestational diabetes, by determination of the plasma concentrations of gastric inhibitory polypeptide (GIP), gut glucagon-like immunoreactivity (gut GLI), insulin, glucagon, and pancreatic polypeptide (PP) following the ingestion of 67 g of triglyceride in late pregnancy and postpartum. Also, the plasma concentrations of free fatty acids (FFA), triglyceride, and glucose were determined. In both groups fasting plasma triglyceride and insulin were increased and PP was decreased. Fasting plasma glucose and gut GLI were decreased in normal pregnancy, but were unaltered in gestational-diabetic pregnancy. Fasting plasma glucagon were unaltered in normal but increased in gestational diabetic pregnancy. In both groups of women the GIP response to triglycerides was impaired in pregnancy. Postpartum, the GIP response was greater in the gestational diabetics than in normal women whereas no difference was found in pregnancy. The other hormones and metabolites responded similarly in pregnancy and postpartum and no difference between normal women and women with gestational diabetes was found. It is concluded that the GIP response to triglycerides is impaired in pregnancy.
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PMID:Gastroenteropancreatic hormones in normal and gestational-diabetic pregnancy: response to oral lipid. 636 71

Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine-induced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway.
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PMID:The endocrine pancreas in pyridoxine deficient rats. 703 87

The gastro-entero-pancreatic (GEP) hormone response to glucose ingestion is considerably altered in pregnancy in normal women and gestational diabetics. In normal women, also the GEP hormone response to protein is changed in pregnancy. In the present investigation, the gastrin, gastric inhibitory polypeptide (GIP), gut glucagon-like-immunoreactivity (gut GLI), insulin, pancreatic glucagon, and pancreatic polypeptide (PP) responses to a protein rich meal in pregnancy and postpartum were studied in 10 women with gestational diabetes. Five of the women were overweight and five were normal weight. Fasting and postprandial gut GLI and PP levels were reduced and insulin levels enhanced in pregnancy. No effect of pregnancy on fasting or postprandial gastrin, GIP, or glucagon levels was found. In pregnancy as well as postpartum, insulin levels were higher in the overweight than in the normal weight patients, whereas the concentrations of the other hormones were similar in the two subgroups of gestational diabetics. It is concluded that the GEP hormone response to a protein rich meal is influenced by late pregnancy in gestational diabetics in the same way as in normal women. The physiological consequences of the findings are not known in detail as yet but they may be important to carbohydrate metabolism and gastrointestinal physiology in pregnancy.
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PMID:Gastro-entero-pancreatic hormones in gestational diabetes: response to a protein rich meal. 711 58

Diabetes mellitus with its resulting derangement of various metabolic fuels, carbohydrates, amino acids, lipids, and ketones has the potential to adversely affect the developing fetus. Therefore, strict glycemic control in pregnancy has become the standard of care in modern obstetrics. A considerable amount of research has been undertaken into the metabolic changes that occur during pregnancy in both women with insulin-dependent diabetes and gestational diabetes. This paper will review current research in normal and diabetic pregnancies both in the fasting and fed states as well as during episodes of hypoglycemia. In normal pregnancy insulin secretion increases throughout gestation whereas peripheral insulin sensitivity is decreased. Fasting levels of plasma glucose are reduced by approximately 10 per cent during the first trimester. Maternal amino acid levels are also reduced in normal pregnancy, although cholesterol and triglyceride levels are increased, most dramatically in the second trimester. As gestation advances, progressively increasing amounts of insulin antagonistic hormones are secreted by the placenta. This leads to gestational diabetes in 2 to 3 per cent of women who exhibit hyperglycemia despite an increased insulin response to oral glucose as well as an increased insulin/glucagon ratio. In insulin dependent diabetes mellitus, the insulin-deficient state results in fasting and postprandial hyperaminoacidemia, hyperlipidemia, and hyperglycemia. These metabolic changes and the resulting hyperglycemic milieu can lead to fetal macrosomia that will result in maternal and fetal morbidity. Therefore, normalization of these fuels with the use of intensive insulin regimens is the goal of therapy during pregnancy.
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PMID:Metabolic changes in diabetic and nondiabetic subjects during pregnancy. 813 54

The present study assessed the possible role of oxytocin in the deterioration of glucose tolerance in gestational diabetes. Plasma levels of oxytocin, insulin, glucagon and glucose were measured at the time of a 400-kcal breakfast meal tolerance test in 12 women with gestational diabetes and 12 normal pregnant women in the third trimester. The gestational diabetic women had higher basal levels of insulin and an enhanced, delayed and prolonged insulin response to the breakfast. The same differences occurred in the glucose levels. There was no significant difference in the glucagon levels between the two groups. In the normal pregnant women, a significant (p < 0.05) though small rise in glucagon levels occurred 30 min after the ingestion of the breakfast. Oxytocin levels were not affected by the breakfast, and there was no clear difference between the two groups. The metabolic differences between the normal pregnant and gestational diabetic women were not related to any differences in oxytocin levels. In conclusion, we found no evidence of a role of oxytocin in the alteration of glucose metabolism in women with gestational diabetes. However, since alterations in oxytocin levels of possible significance for an impaired glucose tolerance are found in type 1 diabetic and extremely obese patients, further studies are needed in women with gestational or manifest diabetes.
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PMID:Is oxytocin involved in the deterioration of glucose tolerance in gestational diabetes? 822 52

We studied the prevalence of mitochondrial gene mutations in subjects with insulin-dependent diabetes mellitus (IDDM) in a Chinese population living in Taiwan. Eighty-four subjects with insulin-dependent diabetes mellitus and 105 unrelated normal controls were recruited in the present study. Both an A-to-G mutation at position 3243 and a mutation at position 8,344 of the mitochondrial DNA were screened by polymerase chain reaction-restriction fragment length polymorphism methods and confirmed by direct DNA sequence analysis. The insulin secretory response was assessed by the C-peptide response to glucagon administration. Among 84 IDDM patients, two (2.4%) subjects were found to carry the 3,243 nucleotide pair (np) mutation. There was no np 8,344 mutation in this series. Of the two subjects carrying a mitochondrial gene mutation, case 1 manifested initially as gestational diabetes mellitus. Manifestation of case 2 was consistent with MELAS, a syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes. The pancreatic beta cell reserve was reduced, as the glucagon-stimulated C-peptide response was very low in these two cases. HLA genotyping studies revealed that case 2 carried DRB1*0301-DQA1*0501-DQB*0201/ DRB1*0405-DQA1*0301-DQB1*0302, which was the most susceptible genotype to IDDM in our population. Anti-GAD65 antibody was also positive in this patient. In addition to the nuclear genes, a defective mitochondrial gene might contribute to some of the clinical cases with IDDM.
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PMID:Mitochondrial gene mutations in patients with insulin-dependent diabetes mellitus in Taiwan. 883 Mar 30

The presence of amyloid deposits in the pancreas was first described at the beginning of the 20th century. However, it was not until 1987 that the structure of the amylin molecule was identified. Amylin is a 37-amino-acid peptide hormone that is co-secreted with insulin by the pancreatic beta-cells in response to a nutrient stimulus. It is deficient in patients with Type 1 diabetes and elevated in patients in the early stages of Type 2 diabetes, a condition which is characterized by hyperinsulinaemia. Elevation of plasma amylin levels has also been described in patients with impaired glucose tolerance, obese subjects and in pregnant women with both normal glucose tolerance and gestational diabetes mellitus. However, it appears that deficiencies of amylin secretion appear before those of insulin in patients in the later stages of Type 2 diabetes. Early experimental studies suggested that amylin inhibits basal insulin secretion, and induces insulin resistance in skeletal muscle, leading to the hypothesis that it has a role in the aetiology of Type 2 diabetes. However, a number of more recent experimental studies have indicated that amylin is a third active pancreatic islet hormone that works with insulin and glucagon to maintain glucose homeostasis. Amylin appears to regulate glucose inflow to the circulation by influencing the rate of gastric emptying, and thus the rate at which meal-derived glucose enters the system, and also by inhibiting glucose release and hepatic glucose production in the postprandial period.
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PMID:Amylin: history and overview. 921 23

Diabetes of the mother during pregnancy induces structural and functional adaptations in the fetal endocrine pancreas. We have previously shown in our experimental rat model, that the impact of this abnormal intra-uterine milieu leads, in the adult offspring, to a disturbance of the glucose homeostasis and to the development of gestational diabetes. The aim of the present work is to investigate wether these functional differences can be explained by structural differences at the level of the endocrine pancreas. Therefore the size and the structure of the endocrine pancreas, as well as the contribution of the insulin-, glucagon-, somatostatin- and PP-cells, were investigated morphometrically in the adult youngsters of mildly and of severely diabetic mothers, since both display a disturbed glucose tolerance but with divergent characteristics. Also the adaptation of their endocrine pancreas to pregnancy was measured and compared to that of a control pregnancy. In the offspring of mildly diabetic mothers, the size of the endocrine pancreas and the distribution of the islets of Langerhans are normal. Also the doubling of the endocrine mass during pregnancy is similar to controls. The high proportion of A-cells, especially in relation to a normal B-cell mass and the low amount of PP-cells, might play a role in the impairment of the insulin response in these animals and in the development of gestational diabetes. In the offspring of severely diabetic mothers a clear hypertrophy of the endocrine pancreas is noted, which is mainly due to the presence of numerous small islets and which does not increase further during pregnancy. In these animals, the size of the endocrine pancreas and of the B-cell mass have reached 'pregnant' values without pregnancy, which coincides with an exaggerated insulin output and peripheral insulin resistance, as during normal pregnancy. No further increase in islet mass is seen during pregnancy, which is associated with gestational diabetes.
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PMID:The endocrine pancreas in virgin and pregnant offspring of diabetic pregnant rats. 934 41

Gestational diabetes is a disease appearing in many forms. Up till now the etiopathogenesis was not clearly defined. It has been suggested that counterregulatory of pregnancy or diminished B-cells could the major contributory factors. The aim of the present study was to retrospective verify the diagnoses of gestational diabetes. The investigation was carried out in 42 women aged 25-39 yrs, mean age 30 +/- 6 yrs. Diabetes was diagnosed in the 2nd, and 3rd, trimesters of pregnancy, 30 women were treated by diet only, 25 kcal/kg b.w. depending on weight, and 12 patients had intensified insulin therapy of mean daily dose 18 +/- 8 U. Three to nine months after delivery a glucose tolerance test as well as estimation of C-peptide and insulin concentration by RIA in basic conditions and after administration of 1 mg of glucagon were performed. In the group of women treated by diet only, normal values of glycaemia in glucose tolerance test were observed. C-peptide concentration measured before administration of glucagon was 1.15 +/- 0.49 ng/ml and after administration of 1 mg of glucagon was 3.14 +/- 1.44 ng/ml. In the majority of patients treated during pregnancy with insulin the results of oral glucose tolerance test were pathological. The concentrations of C-peptide in the test with glucagon were significantly lower (0.33 +/- 0.16 and 0.38 +/- 0.32 ng/ml). The concentrations of insulin were much lower in comparison to women treated with diet and healthy controls, these results suggest that, if gestational diabetes could be controlled by diet only, disturbances of carbohydrate metabolism would disappear, however, if insulin therapy was necessary during pregnancy, disturbances of the carbohydrate metabolism would be prolonged.
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PMID:[Peptide C and insulin after delivery in women with gestational diabetes]. 941 18

This study found that early postnatal hypoglycaemia was mainly induced by foetal hyperinsulinaemia, in close relation to maternal hyperglycaemia, even in well-controlled pregnancies of 59 mothers with insulin-treated diabetes mellitus, 29 with insulin-dependent diabetes mellitus and 30 with gestational diabetes mellitus. Ten of the newborn children (17%) had a blood glucose concentration below 1.0 mmol l(-1) at 2 h postnatally. Cord insulin-like growth factor-I or glucagon concentrations were not related to the early decline of blood glucose.
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PMID:Early postnatal hypoglycaemia in newborn infants of diabetic mothers. 947 19


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