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

Thirteen obese children and matched controls were fed a mixed meal, and responses were evaluated at fixed intervals for glucose, insulin, and gastric inhibitory polypeptide (GIP). The obese children were evaluated before and within 48 h after completion of a 5-mo exercise training program (ETP). The ETP included three aerobic exercise sessions per week and modest diet restrictions. Caloric expenditure was increased by approximately 300 kcal/exercise session. Weight gain was minimal over the 5 mo. An unexpected increase in GIP response and improved insulin tolerance were recorded for the obese children post-ETP. GIP values were higher (P less than 0.05) at 30 and 60 min and led to a highly significant elevation (P less than 0.01) of the integrated GIP response for post-ETP obese versus both pre-ETP and normal-weight controls. Insulin values were lower (P less than 0.05) at 30 and 60 min and led to a lower integrated insulin response (P less than 0.0585) for post-ETP obese children. However, the obese children continued to secrete more insulin (P less than 0.05) than normal-weight controls. Glucose tolerance, similar for pre-ETP obese subjects and controls, did not change in post-ETP children. Exercise-induced improvement in glucose utilization in these obese children was associated with an increase in GIP secretion. This contrasts with reports that calorie restriction will improve glucose utilization with decreased insulin and GIP secretion. The study demonstrates a previously unreported uncoupling of GIP and insulin secretion and suggests shifts in peripheral tissue sensitivity to insulin-induced glucose uptake. These shifts may, in part, be influenced by GIP.
Diabetes 1986 May
PMID:Exercise adaptation responses for gastric inhibitory polypeptide (GIP) and insulin in obese children. Possible extra-pancreatic effects. 351 34

Peripheral venous plasma insulin and C-peptide concentrations were measured in 10 healthy volunteers, given either 100 g glucose orally or sufficient intravenous (i.v.) glucose to produce similar glucose concentrations when measured in arterialized blood. The incremental areas under both the insulin and C-peptide curves were significantly increased after oral as compared with i.v. glucose administration by 229% and 138%, respectively. Arteriovenous plasma glucose differences were higher after oral glucose administration and were positively correlated with plasma insulin concentrations. Plasma gastric inhibitory polypeptide (GIP) and insulin concentrations were measured in seven healthy volunteers given oral glucose loads ranging from 25 to 200 g. Both the magnitude and duration of the GIP and insulin responses after oral glucose ingestion were dose dependent. These results suggest that the main cause of the increase in peripheral insulin levels after large oral carbohydrate loads is augmented insulin secretion rather than reduced hepatic extraction, indicating the possibility that an enteroinsular factor does exist, in accordance with the "incretin" concept. They also emphasize the need to document both arterial and venous glucose concentrations for the correct interpretation of experiments investigating glucose homeostasis.
Diabetes 1986 May
PMID:Insulin and C-peptide levels after oral and intravenous glucose. Contribution of enteroinsular axis to insulin secretion. 351 35

The function of the entero-insular axis and abnormalities of circulating gastric inhibitory polypeptide (GIP) were examined in mice for 40 days after induction of streptozotocin diabetes. Compared with untreated controls, streptozotocin diabetic mice exhibited marked hyperglycaemia and hypoinsulinaemia, with impaired body weight gain, lipoatrophy, hyperphagia, intestinal hypertrophy, polydipsia and renal hypertrophy. Plasma GIP concentrations were elevated in fed but not fasted streptozotocin diabetic mice, and oral fat evoked a greater GIP response than control mice. In spite of marked hyperglycaemia, fat-stimulated GIP release did not raise plasma insulin in streptozotocin diabetic mice. Neither oral nor intraperitoneal glucose produced a significant insulin response in streptozotocin diabetic mice, although oral glucose resulted in a smaller change in glycaemia. The results indicate that streptozotocin diabetes in mice is associated with ineffectiveness of the entero-insular axis, despite elevated GIP concentrations, which are probably mediated through hyperphagia and defective feedback inhibition by insulin on intestinal K cells.
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PMID:Gastric inhibitory polypeptide and the entero-insular axis in streptozotocin diabetic mice. 354 33

Seven subjects with non-insulin-dependent diabetes mellitus were studied prior to and after 1 month of treatment with gliclazide, 80 mg twice daily. Individuals attended for a standard breakfast test meal (10 kcal/kg) on three occasions--prior to therapy, first day of therapy, and 30th day of therapy. Blood samples were collected between 0 and 240 min post-prandially and assayed for glucose, insulin, C-peptide, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide (GIP), and gastrin. Following gliclazide, fasting and post-prandial glucose levels were significantly improved. An increase in post-prandial insulin and C-peptide levels was noted on the first treatment day and values remained elevated for the study period. GIP and other measured peptide hormones were unchanged. These data suggest that gliclazide asserts its hypoglycaemic effects by promoting insulin release, and has no detectable effect on other enteropancreatic hormones.
Diabetes Res Clin Pract
PMID:No effect of gliclazide on gastric inhibitory polypeptide (GIP) in type II diabetes. 359 34

The changes in plasma concentrations of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal were examined in 21 normal subjects and 15 Type 1 (insulin dependent) diabetic patients 7 days, 14 days, and 3, 6, 9, 12, and 18 months after time of diagnosis. During the first 4 tests significantly lower plasma IR-GIP concentrations were found in the diabetic patients after the standard meal. At 9 months and during the remaining tests there was no difference in IR-GIP concentrations between the diabetic and the normal subjects. The IR-GIP response was normalized faster if the diabetic patients were treated with initial short term intensive insulin therapy than if they were treated conventionally with 1 or 2 daily injections of insulin. beta-Cell function, evaluated by the C-peptide response to the meal, increased significantly during the first 3 months. After 3 months maximal beta-cell function was found while the corresponding IR-GIP responses were significantly lower than those of the normal subjects. Thereafter beta-cell function declined gradually and significantly, coinciding with the normalization of the IR-GIP response. No individual covariation between IR-GIP and beta-cell function during the 18 months was found in any patient. The IR-GIP response to a meal was diminished at the onset of Type 1 (insulin dependent) diabetes mellitus. After the start of insulin therapy the response improved, perhaps as a function of the quality of metabolic control, and within a year it was comparable to that of normal subjects. Lack of endogenous GIP therefore does not explain the diminished beta-cell function in Type 1 diabetes a few months after onset of the disease. No causal relationship between the changes in beta-cell function and IR-GIP during the first 18 months after the onset of the disease seems to exist.
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PMID:Immunoreactive gastric inhibitory polypeptide response to a meal during the first eighteen months after diagnosis of type 1 (insulin dependent) diabetes mellitus. 388 May 59

Eight fasting patients with non-insulin-dependent diabetes (NIDD) and six healthy controls were given an intravenous infusion of porcine gastric inhibitory polypeptide (GIP). During the GIP infusion mean plasma pancreatic polypeptide level increased significantly in both groups, whereas the mean serum insulin level increased in the NIDD group only, indicating a more important role for GIP in these patients than in healthy subjects.
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PMID:Effects of intravenously infused porcine GIP on serum insulin, plasma C-peptide, and pancreatic polypeptide in non-insulin-dependent diabetes in the fasting state. 389 Jan 39

Experimental and clinical work over the last 6 years has confirmed and broadened, but also challenged, the incretin concept. The nervous component of the entero-insular axis is still poorly defined, especially the peptidergic nerves, of which several contain insulinotropic regulatory peptides. The incretin effect is preserved after complete denervation of the porcine pancreas. Type 2 (non insulin-dependent) diabetic patients have a significantly decreased incretin effect. GIP (gastric inhibitory polypeptide; glucose dependent insulin releasing peptide) remains the strongest incretin factor. Its secretion depends on the absorption of nutrients. However, the correlation between the GIP response and disturbances of the entero-insular axis in some gastrointestinal diseases and, in particular, Type 2 diabetes, is poor. Furthermore, physiological concentrations of exogenous GIP do not produce fully the incretin effect and injection of GIP antibodies does not abolish the incretin effect. This suggests the existence of additional humoral incretin factors. On the other hand, GIP seems to have direct metabolic effects independent of its insulinotropic activity. The incretin effect of oral glucose is smaller if plasma levels of C-peptide rather than insulin are measured. However, decreased hepatic extraction of insulin after glucose ingestion only accounts partially for the incretin effect. GIP is unlikely to be the gut factor which regulates hepatic insulin extraction.
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PMID:New developments in the incretin concept. 390 45

Serum glucose and gastric inhibitory polypeptide (GIP) responses during mixed test meals and primed continuous infusion of insulin using the insulin clamp technique were studied in nine patients with noninsulin-dependent diabetes mellitus (NIDDM) before and after vigorous insulin treatment. Fasting serum glucose concentrations fell an average of 167 mg/dl (P less than 0.001), and there was a 67% reduction (P less than 0.001) in the postprandial glucose response. Mean hemoglobin A1c declined and paralleled the fall in serum glucose concentrations (9.2 +/- 0.5% to 5.9% +/- 0.3%; P less than 0.01). This improvement in glycemic control, however, was not associated with any appreciable change in GIP secretion. Basal and meal-stimulated serum GIP levels were not reduced after intense insulin therapy. Furthermore, hyperinsulinemia at physiological (100 microU/ml) and superphysiological (1000 microU/ml) levels failed to reduce GIP secretion before and after insulin therapy. Before insulin therapy, seven patients had elevated basal GIP levels and five had increased GIP levels after meals compared to values in nondiabetic subjects. Insulin administration did not alter these elevated GIP levels. These findings suggest that the increased meal-stimulated GIP secretion in some patients with NIDDM is not due to a failure of insulin feedback on GIP secretion.
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PMID:Increased gastric inhibitory polypeptide is not reduced in patients with noninsulin-dependent diabetes mellitus treated with intense insulin therapy. 390 66

To examine the effects of long-term elevation of plasma gastric inhibitory polypeptide (GIP), the responses to parenteral (PA) or enteral (EA) alimentation were studied in conscious rats with duodenal and venous cannulae. A weight-maintaining liquid diet (84% as glucose, 16% as amino acids) was infused at a constant rate for 6 days by either route, and daily blood samples were taken. A subset of animals receiving PA also received porcine GIP with the infusate (PA plus GIP; plateau plasma immunoreactive GIP, IRGIP, 610 +/- 120 pg/ml). With PA, plasma IRGIP did not change from basal levels, whereas with EA IRGIP rose to virtual plateau levels (mean 530 +/- 110 pg/ml). In the steady state, plasma immunoreactive insulin (IRI) was significantly lower with EA (mean, 153 +/- 5 microU/ml) than with PA (mean, 226 +/- 15 microU/ml), which in turn was lower than with PA plus GIP (mean, 375 +/- 23 microU/ml, P less than 0.001 by ANOVA). A similar ranking of plasma glucose levels occurred in the steady state, with means of 113 +/- 7 (EA), 126 +/- 3 (PA), and 184 +/- 9 (PA plus GIP) mg/dl (P less than 0.001 by ANOVA). To assess the response to transient hyperglycemia in the steady state, an intravenous glucose bolus was given to each group on the fifth day. Peak plasma IRI levels did not differ among the three groups; however, the glucose disappearance rate was significantly slower with PA plus GIP compared with either EA or PA.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1985 Nov
PMID:Effects of gastric inhibitory polypeptide in the response to prolonged parenteral or enteral alimentation in rats. 393 Mar 23

Serum gastric inhibitory polypeptide (GIP), insulin, and glucose responses to either a 75-g oral glucose challenge or a 500-cal liquid test meal were determined in 141 Caucasians and American Indians. The Caucasians were normal weight, averaging 101 +/- 3% (+/-SEM) ideal BW (IBW), or were obese (168 +/- 21% IBW) and had normal glucose tolerance (n = 77), impaired glucose tolerance (IGT; n = 12), or noninsulin-dependent diabetes mellitus (NIDDM; n = 19). The American Indians were all obese (144 +/- 6% IBW) and had either normal glucose tolerance (n = 22) or NIDDM (n = 11). In all study subjects, including obese individuals with and without glucose intolerance, diabetic patients both thin and obese, and lean subjects with impaired glucose tolerance, fasting serum insulin and GIP, and incremental glucose, insulin, and GIP were greater than they were in normal lean subjects, especially during the first hour of the tests. Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. Exceptions were two groups with the most severe diabetes in whom incremental insulin values after oral glucose were only 70% (thin Caucasians) and 110% (obese Indians) that of lean normal subjects. The smallest differences in GIP responses occurred between lean normal subjects and obese nondiabetic Caucasians tested with either a meal or oral glucose, whereas American Indians consistently had the greatest insulin and GIP responses to the tests. High fasting GIP and exaggerated GIP increments in response to nutrients could be attributed to neither obesity nor diabetes alone nor to the type of nutrient used to stimulate its release, but, instead, may be genetic or dietary in origin or may be due to other as yet unidentified factors. High basal GIP and exaggerated nutrient-stimulated GIP release were associated with hyperinsulinemia, except in the most severe diabetic patients. These observations suggest that exaggerated GIP release, along with a greater rise in serum glucose in response to nutrients, may play a role in the pathogenesis of the hyperinsulinemia of obesity and early NIDDM.
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PMID:Gastric inhibitory polypeptide responses to nutrients in Caucasians and American Indians with obesity and noninsulin-dependent diabetes mellitus. 400 8


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