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

The entero-insular axis comprises direct substrate stimulation of the islet cells by the absorbed nutrients and signal transmission by endocrine factors and nerves. The extent of neural influences has not yet been evaluated. GIP is the main incretin candidate. GIP release is dependent on nutrient absorption. Therefore, GIP abnormalities occur in a large number of gastrointestinal and metabolic diseases. These secondary changes are rarely of clinical significance. GIP hypersecretion may, however, contribute to the increased lipogenesis in obesity and the hypoglycemia in the late dumping syndrome. In type II diabetes hyper- and hyposecretion of GIP has been found but no correlation between GIP and insulin response. GIP abnormalities are not identical with disturbances of the entero-insular axis. These can only be evaluated by estimating the incretin effect (comparing the insulin response to oral glucose with the insulin response to an isoglycaemic iv glucose infusion). A decreased incretin effect has been observed in patients with jejuno-ileal bypass and in type II diabetes. In neither condition was a correlation found between incretin effect and GIP response. It is concluded that disturbances of the entero-insular axis are rarely explained by GIP abnormalities. Therefore, other humoral gut factors must exist. Also the neural part of the entero-insular axis requires exploration in health and disease.
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PMID:Disturbances of the entero-insular axis. 635 14

We describe the results of metabolic studies in a 17-year-old woman with diabetes mellitus which was the initial manifestation of idiopathic chronic calcifying pancreatitis (CCP). These studies were done on 2 occasions, 5 months and 5 years after the onset of diabetes, when her diabetes could be managed by glibenclamide and insulin, respectively. Five months after the onset of diabetes, oral glucose produced a small increase in insulin and a paradoxical rise in both glucagon immunoreactivity (GI) and growth hormone (GH). BY contrast, arginine-stimulated responses of the three hormones were normal. No increase in GI and a blunted rise in GH resulted from an insulin-induced decrease in blood glucose. Five years later, when CCP was demonstrated by roentogenologic examinations and tests of pancreatic exocrine function, oral glucose was followed by a flat and depressed response of C-peptide immunoreactivity and a markedly elevated response of gut glucagon-like-immunoreactivity (gut GLI). There were delayed and extremely low responses of pancreatic polypeptide to a test meal, irrespective whether or not her diabetes required treatment with insulin. These results demonstrate that CCP can cause diabetes in adolescents, as it does in adults, and that the adolescent woman described here had impaired responses of PP and gut GLI as well as insulin, GI and GH, especially to changes in blood glucose levels.
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PMID:Diabetes mellitus secondary to idiopathic chronic calcifying pancreatitis in an adolescent woman. 635 71

In 1980 we described an in vivo method for estimating the rate of glucose uptake among selected tissues during an acute insulin response. The method was based upon the same principles as Sokoloff's 2-deoxyglucose (2DG) method. We now report further examination of the basic assumptions of the model and validation of its general applicability by comparing the response of brain and other tissues to prolonged insulin infusion (while glucose is held constant) with their response to a single injection of insulin. The method provides a reproducible estimate of relative insulin response in any tissue that can be anatomically separated at death. Tissues that are minimally sensitive to insulin such as spleen, lung, skin, and gut do not display increments in the calculated value for net rate of tissue uptake of 2DG. Insulin-sensitive tissues display increased rates of uptake that are characteristic for each specific tissue, ranging in magnitude from 1.7- to 17.9-fold over basal among an array of insulin-sensitive tissues. The duration of a unit response to a sub-maximal dose of insulin also varied among the tissues, persisting for 20-30 min after plasma insulin had returned to basal in heart and for 10-20 min in the other insulin-sensitive tissues. The method provides a reproducible measure of glucose metabolism in vivo and has been validated as a means of quantifying relative insulin sensitivity among the peripheral tissues. During steady-state conditions with plasma glucose held constant, brain glucose metabolism was unaffected by a 60-min infusion of insulin.
Diabetes 1984 Feb
PMID:A [3H]2-deoxyglucose method for comparing rates of glucose metabolism and insulin responses among rat tissues in vivo. Validation of the model and the absence of an insulin effect on brain. 636 68

The influences of major pancreas resection upon gastric acid secretion and gut hormones were studied in dogs with Heidenhain pouches. Immediately after resection of 90% or more of the entire pancreas, diabetes occurred with an abrupt decrease in insulin and glucagon secretion, and a marked increase in gastric acid output, though gastrin secretion decreased and secretin secretion increased, as after total pancreatectomy. Six weeks or more after resection of 70 to 90% of the entire pancreas, so-called Sandmeyer's diabetes occurred as a consequence of a decrease in insulin secretion and an increase in glucagon secretion from the remnant pancreas. Gastric acid output decreased markedly, and gastrin secretion also decreased. After resection of less than 70% of the entire pancreas, diabetes did not occur during 66 weeks of the longest observation period after surgery. Gastric acid output, secretion of gastrin and secretin did not change after surgery. These results suggest that gastric hypersecretion occurs after total pancreatectomy and resection of 90% or more of the entire pancreas, and it is related to pancreatic exocrine insufficiency and that gastric hyposecretion occurs after resection of 70 to 90% of the entire pancreas, and it may be related to hypersecretion of glucagon and somatostatin.
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PMID:[Gastric secretion after major resection of the pancreas, with special reference to gut hormones and gastric acid secretion in Sandmeyer's diabetes]. 637 80

The involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemic conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.
Diabetes 1984 Jun
PMID:Gastric inhibitory polypeptide (GIP) and insulin release in the obese Zucker rat. 637 59

Verapamil has previously been found to inhibit insulin release from pancreatic beta-cells in laboratory animals. In our department, however, both oral pretreatment with verapamil for one week and a 3-hour iv infusion of the drug improved the tolerance to oral glucose in type II diabetics without affecting insulin release. It failed, however, to potentiate the hypoglycaemic effect of oral glibenclamide therapy in patients with type II diabetes. Since iv infusion of verapamil left the portal vein glucose response to glucose ingestion unaffected in normoglycaemic patients (being portal vein catheterised for diagnostic purposes), it seems unlikely that the hypoglycaemic effect of verapamil could have been due to reduced glucose absorption from the gut. More likely is that verapamil, in the diabetic patients, influenced metabolic processes inside the hepatocytes that are of importance for glucose homeostasis. In-vitro experiments have shown that calcium affects factors of importance for the glucose metabolism. Accordingly, calcium triggers the stimulus-secretion coupling process which leads to insulin release from the pancreatic beta-cells (1). Calcium also tightens cell membranes, thereby decreasing their permeability to various substances, including glucose (2). Finally, calcium mediates cellular responses to glucagon stimulation (3,4) and thus affects the hepatic glucose output. Calcium apparently influences glucose metabolism by several pathways and different overall effects on the blood glucose concentration may be forthcoming depending on which of these pathways is the dominating one.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of verapamil on glucose tolerance. 637 85

Diabetes mellitus can affect every organ system, including large and small blood vessels, eyes, nerves, kidneys, and the gastrointestinal (GI) tract. We reviewed recent knowledge concerning the impact of diabetes on the gut. While the incidence of GI tract complications is usually considered relatively low, functional alterations have been demonstrated at every level in the gut and account for considerable morbidity in the diabetic population.
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PMID:Gastrointestinal tract complications of diabetes mellitus. Pathophysiology and management. 637 14

The myenteric plexus is the neuronal complex that regulates the motility of the gut; a brief review of its pathology is presented in this paper as well as a tentative etiopathogenetic classification. Disorders of gut innervation include congenital (e.g. Hirschsprung's disease) or acquired diseases; the latter can be idiopathic or related to a more general pathological involvement of the whole organism as in the case of bacterial toxins, diabetes mellitus, Riley-Day disease and primary orthostatic hypotension. In view of the fundamental similarity of the myenteric plexus to the central nervous system, the study of this organ can be useful both for diagnosis of degenerative diseases of the central nervous system (i.e. via rectal biopsy) and for gaining a better etiopathogenetic insight into peripheral and central nervous system disease.
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PMID:Neurological disorders of the myenteric plexus: a review. 639

Amino acid concentrations in whole blood, liver, kidney, skeletal muscle, and brain were measured and arteriovenous differences calculated for head, hindlimb, kidney, gut, and liver in control and streptozotocin-diabetic rats. In the control rats, glutamine was released by muscle and utilized by intestine, intestine released citrulline and alanine, liver removed alanine, and the kidneys removed glycine and produced serine. In diabetic rats, the major changes from the pattern of fluxes seen in the normal rat were the release of many amino acids from muscle, with glutamine and alanine predominating, and the uptake of these amino acids by the liver. Glutamine removal by the intestine was suppressed in diabetes, but a large renal uptake of glutamine was evident. Branched-chain amino acids were removed by the diabetic brain, and consequently, brain levels of a number of large neutral amino acids were decreased in diabetes.
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PMID:Interorgan metabolism of amino acids in streptozotocin-diabetic ketoacidotic rat. 640 31

Specific and total activities of the disaccharidases, sucrase, maltase, and lactase are increased in mucosa of the small intestine of the streptozotocin diabetic rat. Because disaccharidases are essential for terminal digestion of carbohydrate, and disaccharidase deficiency is a common clinical problem, understanding the mechanisms regulating disaccharidase activity is important. In normal animals, disaccharidase activities are determined by route of feeding and are decreased by parenteral feeding. The indirect exocrine, endocrine, neurocrine, and paracrine functions of the gastrointestinal tract that are dependent on feeding via the gut are greatly decreased in parenteral as compared with enteral feeding. Hormone secretion by the gut and the pattern of response after feeding may be abnormal in diabetes and might be regulatory for disaccharidases. We tested the hypothesis that the elevated intestinal disaccharidases in diabetes are dependent on enteral feeding. Streptozotocin-injected rats (diabetics) and vehicle-injected rats (controls) were fed rat chow ad libitum for 4 days. A subset of control and diabetic animals was then killed to determine disaccharidase activity of the jejunum at the start of pair-feeding the elemental diet. The remaining animals were fed 60 cal/day of glucose, amino acid (Travasol), and electrolyte solution either intragastrically or intravenously for 4 days. Specific and total activities of disaccharidases were greater in diabetics than in controls under all feeding conditions. In controls, the pattern of activity of disaccharidase specific activity was initial greater than intragastric greater than intravenous. In diabetics, disaccharidase specific activities did not differ among groups. In both controls and diabetics, mean mucosal mass was highest initially; intermediate with intragastric feeding; and lowest with intravenous feeding. In both controls and diabetics, total disaccharidases decreased from initial to intragastric to intravenous. We conclude: (1) disaccharidase specific activity in controls is sensitive to feeding route and nature of diet, but is nearly independent of these factors in diabetics; (2) total disaccharidase activities respond to feeding stimuli in parallel with changes in mucosal mass in both controls and diabetics; and (3) the lack of feeding effect on the elevated specific activities of disaccharidases in diabetes suggests that this elevation is a response to the diabetic state and is independent of enteral factors such as luminal nutrition and gastrointestinal hormones.
Diabetes 1983 Mar
PMID:Elevated intestinal disaccharidase activity in the streptozotocin-diabetic rat is independent of enteral feeding. 640 7


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