Augmentation of Insulin Secretion by a Non-Nutrient Drink

Goldberg, Neil; Wingert, Terence D.; Levin, Seymour R.; Adachi, Robert I.

doi:10.1016/s0016-5085(19)30501-3

Cited by 15 publications

(6 citation statements)

References 29 publications

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“…However, glucagon levels were not significantly different in all groups in the present study. This result was in agreement with the report of Goldberg et al ( 5 ) that glucose-induced suppression of glucagon was not affected by ingestion of the drink (3% mannitol) in the human. Gastrin is also known to enhance glucose-induced insulin release ( 1, 3).…”

Section: Intestinal Osmolality and Insulinsupporting

confidence: 94%

“…Goldberg et af. ( 5 ) , Shima et al (6), and we (7) have reported that ingestion of a non-nutrient drink augments insulin secretion in response to a subsequent intravenous glucose load in humans and rats, suggesting that intestinal mechanical stimulation and/or osmolality may play a component role in insulin release. However, the effect of intestinal osmolality on insulin secretion remains to be further elucidated.…”

Section: Tinal Factors and Several Investigators ( 1-4) Havementioning

confidence: 80%

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Effect of Intestinal Osmolality on Insulin Secretion to Subsequent Intravenous Glucose or Arginine in the Rat

Ikeda

Fujiyama²,

Hoshino³

et al. 1990

Experimental Biology and Medicine

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To elucidate the effect of intestinal osmolality on insulin secretion, we investigated insulin response to a subsequent intravenous infusion of glucose or arginine after intragastric or intraduodenal mannitol or NaCl instillation in the rat. After anesthesia with intraperitoneal pentobarbital sodium, mannitol solution (10% or 20%) or 2.7% NaCl was instillated into the stomach or duodenum for 5 min at a flow rate of 0.5 ml/min, and 20% glucose (0.5 g/kg) or 10% L-arginine (0.5 g/kg) was infused bolus into the femoral vein 45 min after intestinal instillation. Insulin response to intravenous glucose was significantly higher in the rat with intragastric or intraduodenal mannitol or NaCl infusion than in control rats with intragastric or intraduodenal instillation of distilled water. Insulin response to intravenous arginine was almost the same in all groups. Subcutaneous preadministration of propranolol (0.4 mg/kg), atropine (1.2 mg/kg), or phentolamine (0.8 mg/kg) did not alter the present phenomenon. These results suggest that intestinal osmolality may enhance insulin release to intravenous glucose, but not to arginine in the rat.

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Section: Intestinal Osmolality and Insulinsupporting

confidence: 94%

Section: Tinal Factors and Several Investigators ( 1-4) Havementioning

confidence: 80%

Effect of Intestinal Osmolality on Insulin Secretion to Subsequent Intravenous Glucose or Arginine in the Rat

Ikeda

Fujiyama²,

Hoshino³

et al. 1990

Experimental Biology and Medicine

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“…Levin et al [96] demonstrated incretin effects in a perfused rat gut-pancreas preparation after intraduodenal instillation of electrolyte solutions or mannitol. In man, inges-tion of mannitol has also been shown to augment glucose-induced insulin output [97]. These effects are certainly not due to GIP release, since mannitol or hyperosmolar electrolyte solutions are not capable of releasing GIP [45].…”

Section: Evidence For the Existence Of Additional Insulinotropic Factorsmentioning

confidence: 99%

New developments in the incretin concept

1985

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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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“…Its insulinotropic effect has been demonstrated by numerous authors (TURNER et al, 1974;SCHAUDER et al, 1975;PEDERSON et al, 1 9 7 5~;PEDERSON & BROWN, 1976;CROCKETT et al, 1976). Yet many works mainly performed on animals suggest that it is not the only molecule possessing this type of effect (MOODY, 1977;ZERMATTEN & FELBER, 1978;LEVIN et al, 1979;GOLDBERG et al, 1980;LAURITSEN et al, 1981;EBERT et al, 1979EBERT et al, & 1983. In that manner, partly purified intestinal extracts have an insulinotropic effect in the rat in vitro (MOODY, 1977) and in vivo (ZERMATTEN & FELBER, 1978;EBERT et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

“…GIP antiserum infusions in the rat cannot abolish completely the incretin effect (EBERT et al, 1979;LAURITSEN et al, 1981). Perfusions of isolated rat intestine segments with electrolyte solutions (LEVIN et al, 1979), or oral ingestion of such solutions by man (GOLDBERG et al, 1980) made it possible to demonstrate the existence of insulinotropic substances other than GIP, since the latter is solely secreted after nutrient ingestion (amino acids, carbohydrates and fat) (CLEATOR & GOURLAY, 1975;PEDER-SON et a/., 19756;O'DORISIO et al, 1976;FALKO et al, 1975).…”

Section: Introductionmentioning

confidence: 99%

Influence of Ingested Load on Postprandial Insulin Secretion. Rôle of Gastric Inhibitory Polypeptide (GIP)

Beck

Villaume

1985

Archives Internationales de Physiologie et de Biochimie

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Two standard mixed meals including the same ingredients, and with different caloric values were ingested by 10 normal subjects. The plasma gastric inhibitory polypeptide (GIP) and immunoreactive insulin (IRI) as well as blood glucose (BG) were assayed during these meals at 0 (beginning of the meal) and after 30, 60, 120 and 180 min. BG was not significantly different between the two meals. At 30 min, the GIP peak was significantly higher in the case of the meal with the highest caloric (HC) value (499.5 +/- 112.0 vs. 273.4 +/- 57.5 pg/ml). Insulin was higher as well, although not in a significant way. At 120 min, the IRI was significantly higher (63.0 +/- 9.8 vs. 34.4 +/- 6.2 microU/ml) in the case of the HC meal. The HC meal induced a significantly higher insulinogenic index (0.29 +/- 0.05 vs. 0.14 +/- 0.07 mU litre g-1 ml-1). Integrated IRI and GIP responses of the HC meal were significantly higher than those of the meal with the lowest caloric value (IRI : 7.9 +/- 1.1 vs. 4.9 +/- 0.6 mU ml-1 180 min-1; GIP : 53.3 +/- 20.5 vs. 28.2 +/- 9.9 ng ml-1 180 min-1). The early (30 min) augmentation of IRI secretion after the ingestion of a larger meal is related to the insulinotropic action of the enhanced GIP secretion. The reasons for the late IRI increase are not obvious from this experiment. They might be of neural, nutrient, and/or intestinal origin.

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Augmentation of Insulin Secretion by a Non-Nutrient Drink

Cited by 15 publications

References 29 publications

Effect of Intestinal Osmolality on Insulin Secretion to Subsequent Intravenous Glucose or Arginine in the Rat

Effect of Intestinal Osmolality on Insulin Secretion to Subsequent Intravenous Glucose or Arginine in the Rat

New developments in the incretin concept

Influence of Ingested Load on Postprandial Insulin Secretion. Rôle of Gastric Inhibitory Polypeptide (GIP)

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