Search

To study the postprandial blood glucose and insulin responses to exchangeable amounts of simple and complex carbohydrates, eight non-insulin-dependent diabetic subjects consumed 227 g apple, 280 g orange or 50 g white bread on three separate days. The mean postprandial blood glucose response area to white bread (404 +/- 95 mM x 240 min) was significantly higher compared with orange (131 +/- 34 mM x 240 min; P less than 0.05) and apple (157 +/- 57 mM x 240 min; P less than 0.05). Thr glycaemic indices of the fruits were identical: 44 +/- 13 (orange) and 40 +/- 11 (apple). The low glycaemic response to orange and apple may be ascribed to the high content of fructose which is rapidly cleared and metabolized by the liver, without elevating the blood glucose.

Individual dietary regulation is still an important part of all forms of treatment of diabetes. In insulin dependent diabetes (IDDM) it is rational to advise the patient 1) to arrange his diet so that this results in a low glycaemic response, which implies a relatively high intake of dietary fibre and polysaccharides, 2) to distribute the food into 5-6 daily meals and 3) to consume a low-fat diet. This prevents too pronounced postprandial hyperglycaemia and hypoglycaemia between meals. Simultaneously, insulin sensitivity is increased and not only the insulin requirement but also peripheral hyperinsulinism tend to be reduced. Dietary regulation in IDDM is thus a compensation for the defective synchronization of variations in the plasma levels of glucose and insulin in the present day forms of insulin therapy. Nine out of ten diabetic patients are non-insulin dependent (NIDDM). The great majority are obese, 50% have essential hypertension and just as many have dyslipidaemia (raised serum triglyceride and reduced serum high density lipoprotein (HDL)-cholesterol). The condition is characterized pathophysiologically by insulin resistance in muscle, fat and liver tissue and delayed and frequently reduced glucose-stimulated secretion of insulin. The most important element in dietary regulation in NIDDM is, therefore, reduction of the energy content of the food with the object of achieving and maintaining reduction in weight. Even moderate reduction, in the majority of NIDDM patients, will have the effect that metabolism of carbohydrates and lipids becomes approximately normal on account of considerable increase in insulin sensitivity and to a lesser degree increased secretion of insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

The 29-amino acid neuropeptide galanin occurs in intrapancreatic nerves and inhibits insulin secretion. To study the structure-activity relations of galanin, we examined the effects of pig and rat galanin, three galanin fragments (galanin-(1-11), galanin-(1-16) and rat galanin-(17-29) and four galanin analogues ([Ala2]pig galanin, [Ala2]rat galanin, [D-Trp2]rat galanin and [D-Trp2]galanin-(1-16] on glucose-stimulated insulin secretion from isolated rat islets. Pig and rat galanin and galanin-(1-11) equipotently inhibited glucose-stimulated (8.3 mM) insulin secretion at and above 10(-7) M (P less than 0.05), whereas galanin-(1-16), inhibited insulin secretion at 10(-6) M (P less than 0.01). In contrast, the C-terminal rat galanin-(17-29) and the galanin analogues did not influence insulin secretion. Thus, rat and pig galanin are equipotent in inhibiting glucose-stimulated insulin secretion from rat islets. The active site resides in the N-terminal part of the molecule. Furthermore, the binding of galanin to its receptor depends on structural characteristics governed by the N-terminal position and in particular by the Trp2 residue.

The metabolic changes in connection with fasting, anaesthesia and surgery in diabetic patients and non-diabetic patients are reviewed. Various perioperative forms of treatment are described. The forms of treatment most commonly employed are infusion of glucose-insulin-potassium (GIK) and subcutaneous administration of insulin followed by infusion of glucose (KON). The more intensive GIK regime provides the diabetic patient with a biochemical regulation which resembles that found in non-diabetics. It has not been proved whether this marginal regulation influences the well-being, morbidity or mortality of the patients. In critically ill patients or patients with concurrent diseases, the GIK regime is recommended as this provides optimal regulation of the diabetes. In the remaining patients, local conditions will influence the choice of form of treatment.

Galanin occurs in intrapancreatic nerves and inhibits insulin secretion both in vivo and in vitro. To investigate which part of the galanin molecule accounts for this inhibition, we studied the effect of porcine galanin, four galanin fragments and three galanin analogues with substitutions of the 2nd amino acid in galanin, on glucose-stimulated insulin secretion from isolated rat islets cultured overnight. The islets were incubated for 1 h at 8.3 mM glucose. Porcine galanin1-29 inhibited insulin secretion at dose levels from 10(-8) M to 10(-6) M (p less than 0.001). Also, the galanin fragments GAL1-15, GAL2-29, and GAL3-29 significantly inhibited insulin secretion at and above concentrations of 10(-7) M (p less than 0.001), 10(-8) M (p less than 0.001), and 10(-7) M (p less than 0.001), respectively. Galanin analogues where the 2nd N-terminal amino acid had been changed from tryptophan to tyrosine (GAL-TYR2) or isoleucine (GAL-ILE2) inhibited insulin secretion, as did porcine galanin1-29, whereas after substitution with phenylalanine (GAL-PHE2) no effect was observed. Furthermore, the C-terminal fragment GAL10-29 did not influence insulin secretion. We conclude that the inhibitory action by galanin on glucose-stimulated insulin secretion from normal islets resides in the N-terminal part of the molecule. In contrast, the C-terminal part of galanin apparently does not influence insulin secretion.

To study the glycaemic effect of various Danish bread types in insulin-dependent diabetic subjects (IDDM) we looked at the incremental blood glucose areas after isocaloric meals of grained wholemeal rye bread, wholemeal bread (graham bread) and white bread in seven C-peptide negative diabetic subjects. Furthermore, we evaluated the glycaemic potency of dried fruits by exchanging 40 per cent of the starch of grained wholemeal rye bread as dried figs. Prior to the meal intake the patients had attained normoglycaemia and isoinsulinaemia by means of the artificial pancreas. The four test meals containing 50 g of available carbohydrate were taken in random order. The postprandial blood glucose response areas after whole-meal bread (1037 +/- 113 mM X 180 min) and white bread (1021 +/- 100 mM X 180 min) were significantly higher than that to grained wholemeal rye bread (786 +/- 66 mM X 180 min, P less than 0.05). Exchange of 40 per cent of the complex carbohydrate as grained wholemeal rye bread with simple sugars, such as figs, had no influence on the blood glucose response (786 +/- 66 mM X 180 min vs. 766 +/- 56 mM X 180 min). Constant and identical serum-free insulin levels at 30 mU/l and similar amounts of glucose lost in the urine were found after the four test meals. In conclusion, the difference in extraction rate of wheat in the form of white flour (0, 7) and wholemeal flour (1, 0) was not reflected in the glycaemic responses in IDDM subjects. Grained wholemeal rye bread is a fibre-rich, cheap nutrient which elicits a significantly lower glycaemic response compared to wholemeal and white bread and can be recommended to diabetic subjects.

The present study was carried out to see if either the volume of water or the duration of ingestion time influence the postprandial blood glucose and insulin responses in non-insulin-dependent diabetic (NIDDM) subjects. Small test meals containing 40 g carbohydrate as rye bread (100 g) with butter (10 g) and tomatoes (75 g) were given to 10 NIDDM subjects. The meals were taken in random order with either 90 or 600 mL tap water. The meal with 90 mL tap water was ingested over 10 and 30 min. The glycemic responses to isocaloric meals of large and small volumes were similar (338 +/- 56 vs 384 +/- 67 mmol/L.240 min) as were the insulinemic responses (29,424 +/- 6512 min vs 27,140 +/- 6548 mumol/L.240 min). An extension of eating time from 10 to 30 min did not alter the glycemic (384 +/- 67 vs 370 +/- 54 mmol/L.240 min) or the insulinemic response (27,140 +/- 6548 vs 35,670 +/- 10,245 mumol/L.240 min) in the NIDDM patients.