Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of insulin-dependent diabetic (IDDM) women to breast-feed has been documented, however, there is little information concerning milk composition or factors that influence successful breastfeeding. Placental lactogen and prolactin levels can be normalized during pregnancy with good metabolic control. These hormones affect the readiness of the mammary gland for lactation. Prolactin maintains mammary gland insulin receptors to ensure anabolism. Lactation in IDDM women may be influenced by hyper- or hypoglycemia as women balance their insulin needs. Milk from diabetic animals has decreased lactose, fat, protein and volume and these effects can be reversed with insulin administration. Mature breast milk of IDDM women has increased glucose and sodium and mammary gland lipid metabolism may be impaired. Milk lactose and citrate, markers of lactogenesis II, suggest delayed lactation occurs in diabetic women. Many factors may influence lactation success and breast milk composition of IDDM women. Some of these include: method of delivery, feeding frequency, fetal condition, gestational age, mastitis incidence, metabolic control and maternal dietary intake. Lactation management of the IDDM woman must address these factors.
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PMID:Lactation in insulin-dependent diabetes. 209 Oct 54

Hormonal studies of pituitary-testicular function in insulin-dependent diabetes mellitus were examined at rest and during moderate exercise to assess whether diabetes per se caused abnormalities of nocturnal penile tumescence and androgen function in men with normal sexual function. The present study compared 10 healthy men and eight men with Type I diabetes mellitus in whom normal sexual function was determined by clinical history. Urinary gonadotropin excretion, semen analysis and diurnal variation of serum glucose, prolactin, testosterone and free testosterone were determined in both groups. In addition, the serum levels of testosterone, free testosterone, prolactin, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured at rest, during 45 minutes of exercise on a bicycle ergometer at 50% of the subjects previously determined maximal oxygen uptake (VO2 max) and during a 30-minute recovery period. Nocturnal penile tumescence and parameters of semen analysis were similar in both groups. Urinary FSH excretion and serum FSH were higher (P less than or equal to 0.01) in the diabetic subjects while urinary LH excretion was similar. Diurnal variation of serum prolactin, testosterone and free testosterone were similar in both groups. Exercise produced a significant (P less than or equal to 0.01) increase in maximal free and total testosterone in both groups without changes in serum FSH or LH. Prolactin increased significantly (P less than or equal to 0.01) during exercise in the diabetic group only. We conclude that, for the most part, the pituitary-testicular axis and nocturnal penile tumescence under basal conditions and the pituitary-testicular axis during moderate exercise are similar in healthy males and insulin-dependent diabetic males with normal sexual function.
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PMID:The pituitary-testicular axis at rest and during moderate exercise in males with diabetes mellitus and normal sexual function. 313 19

Prolactin (PRL) is well known for its stimulatory effects on various components of the immune response. Experimentally induced high levels of PRL have been shown to correlate with the worsening of several autoimmune diseases. In contrast, lowering PRL levels may protect from the autoimmune process. We investigated in both sexes of NOD mice a spontaneous model of autoimmune type 1 diabetes, the effects of two drugs, a dopaminergic agonist, bromocriptine (BRC, 10 mg/kg), which is assumed to inhibit PRL secretion, and a dopaminergic antagonist, metoclopramide (MCP, 5 mg/kg), which in contrast stimulates PRL secretion, on the incidence of diabetes, the severity of insulitis, and PRL and glucose levels. Chronic treatment of NOD mice with MCP slightly aggravated development of diabetes. The dopamine antagonist tended to accelerate the onset of diabetes in females and significantly increased the number of islets with peri-insulitis in both sexes. The weak deleterious effects exerted by MCP in NOD mice may be related to its stimulatory action on PRL release. Contrary to the expected results, the dopamine agonist BRC did not protect from autoimmune diabetes. In contrast, the drug appeared to accelerate diabetes onset in males and significantly increased the number of islets showing insulitis in both sexes. This study underlines the complexity of the action of BRC which in NOD mice only transiently inhibits the release of PRL. Moreover, the aggravating actions of BRC may be related to the marked hyperglycemic effect of the drug observed in male and female NOD mice.
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PMID:Attempts to pharmacologically modulate prolactin levels and type 1 autoimmune diabetes in the non-obese diabetic (NOD) mouse. 882 12

The aim of the study was to answer the questions: 1) does the prolactin secretion in the TRH test (0.4 mg i.v.) differ in haemodialyzed patients with diabetes nephropathy in the end stage renal failure in comparison to haemodialyzed chronic renal failure patients with non-diabetic nephropathy and healthy subjects; 2) does the opiate receptors blockade with naloxone (2 mg i.v.) modify the prolactin secretion during the TRH test in those patients. 39 subjects were studied. The patients were divided into three groups: group I: 12 haemodialyzed patients with IDDM and diabetic nephropathy in the end stage renal failure, group II: 15 haemodialyzed chronic renal patients with non-diabetic nephropathy and the control group: 12 healthy persons. The basic prolactin secretion and area over basic value (AOBV) of the prolactin were estimated. Prolactin concentration was measured by LIA. 1) The basic prolactin secretion was significantly higher in the patients with chronic renal failure. 2) The basic prolactin secretion in IDDM patients with diabetic nephropathy in the end stage renal failure treated with haemodialysis was significantly lower than in haemodialyzed patients with chronic renal failure of non-diabetic etiology. 3) TRH and TRH with naloxone caused significant increase of prolactin secretion in all investigated groups, but the increase is significantly lower in chronic renal failure patients than in healthy subjects. 4) Naloxone decreases significantly the prolactin secretion during TRH test only in haemodialyzed patients with chronic renal failure of non-diabetic etiology.
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PMID:[Effects of opiate receptor blockade with naloxone on prolactin (PRL) secretion in patients with diabetes type I (IDDM) with chronic renal failure treated with hemodialysis (HD)]. 912 1

Pregnancy is associated with a depression of the immune inflammatory system, and with increased growth and function of the pancreatic islets of Langerhans. We monitored glucosuria, blood glucose concentration, and lymphocytic infiltration of pancreatic islets in 30 female, 10-wk-old, pre-diabetic nonobese diabetic (NOD) mice divided into 3 treatment groups for 13 wk: group 1, saline; group 2, pregnancy hormones (dexamethasone 4 mg/Kg/day, progesterone 1.7 mg/Kg/day, growth hormone 0.6 mg/Kg/day, prolactin 1 mg/Kg/day, and estradiol 0.05 mg/Kg); and group 3, prolactin alone (1 mg/Kg/day). At sacrifice, the pancreases were fixed in paraformaldehyde and islet infiltration was evaluated. In the saline-treated group (#1) 4/10 mice developed diabetes, while in the hormone treated group (#2) none of the mice developed diabetes. Only 1/10 mice in the prolactin-treated group (#3) developed diabetes during the study. Islets from the hormone cocktail treated group were significantly less infiltrated than islets from the other 2 treatment groups (p <0.001). Thus, the pregnancy hormones protected NOD mice from developing diabetes and significantly reduced or eliminated insulitis and islet infiltration. Prolactin alone had a partial protective effect. The results have implications for prevention of type 1 diabetes and for immune suppression in patients receiving islet cell transplantation.
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PMID:Pregnancy hormones prevent diabetes and reduce lymphocytic infiltration of islets in the NOD mouse. 1184 23