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  • 1
    ISSN: 1432-0428
    Keywords: Guar ; GIP ; glucacon-like immunoreactivity ; enteroinsular axis ; insulin ; glucose ; diabetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Five healthy volunteers and 6 diabetics were given a mixed test meal on two occasions — once with and once without 10 g guar flour. Addition of guar caused a 47% decrease in maximum post-prandial GIP levels, a 48% decrease in blood glucose and a 48% decrease in plasma insulin in normal subjects. In diabetics, addition of guar caused a 30% reduction in maximum post-prandial GIP and 58% decrease in blood glucose. Four normal and 6 diabetic subjects were given a predominantly carbohydrate meal, again with and without 10 g guar. Addition of guar caused a 78% decrease in blood glucose and a 59% decrease in plasma insulin in normal subjects. In diabetics addition of guar caused a 71% decrease in maximum post-prandial plasma GIP and a 68% decrease in blood glucose. Lowering of post-prandial blood glucose, plasma insulin and GIP levels by guar was statistically significant in every case. Addition of guar to the predominantly carbohydrate meal caused a decrease in total plasma GLI in both normal and diabetic subjects but reached statistical significance only in the normal subjects. There was a highly significant correlation (r=0.83; p〈0.0005) between peak post-prandial insulin levels in normal subjects and the corresponding plasma GIP concentration. The reduction in GIP or GLI secretion may, therefore, be partly responsible for the smaller rise in plasma insulin observed in normal volunteers when guar is added to meals.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 16 (1979), S. 235-239 
    ISSN: 1432-0428
    Keywords: GIP ; oral galactose ; insulin secretion ; enteroinsular axis ; induced hyperglycaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The insulinotropic effect of 50 g galactose given orally to 5 normal volunteers on two occasions — once with and once without a period of hyperglycaemia produced by an intravenous glucose infusion — was studied. Oral galactose caused a rise in plasma GIP from fasting levels of 260±50 ng/l (mean ± S. E. M.) to a maximum of 900±65 ng/l 30 min after ingestion, but in the presence of induced hyperglycaemia the GIP response was significantly diminished and delayed (maximum plasma GIP levels 595+110 ng/l at 45 min, p〈0.05). The insulin response to galactose was greatly enhanced by IV glucose (mean area under plasma insulin curve with galactose alone 236.5±66.0, with galactose + IV glucose 451.9+81.6, p〈0.025). The mean rise in plasma galactose was significantly lower in the presence of IV glucose (mean peak level 1.97±0.28 mmol/l with galactose alone, 0.69±0.16 mmol/l galactose + IV glucose, p 〈0.025). Oral galactose caused the release of GIP, which is powerfully insulinotropic in the presence of moderate hyperglycaemia. The lower plasma GIP and galactose levels observed following oral galactose in the presence of IV glucose may be accounted for either by postulating that insulin inhibits the absorption of oral galactose, or that insulin exerts a negative feed-back control on GIP release and accelerates galactose disposition in the body.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: GIP ; insulin ; triolein ; dietary adaptation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Male Wistar rats were pretreated with 3 ml triolein orally for 4 days in addition to their normal diet. A similar control group were allowed free access to normal laboratory food. When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide (GIP) and triglyceride levels were significantly higher in the fat pretreated group. Inhibition of fat-stimulated GIP release by exogenous insulin was demonstrated in the untreated control group (plasma GIP: 663±49 versus 853±92 ng/l, mean ± SEM p 〈 0.025), but pretreatment with an oral fat load abolished this effect (plasma GIP: 1008±95 versus 1116±100 ng/l, p NS). Plasma glucose levels were significantly higher in fat pretreated rats given oral fat and intraperitoneal insulin compared with untreated controls (plasma glucose nadir 2.6±0.48 versus 1.6±0.15 mmol/l, p 〈 0.05). Fat-pretreated rats showed significantly higher insulin and glucose levels compared with the untreated rats when given oral glucose (plasma insulin: 6.2±1.2 versus 2.5±0.59 n.g/l, p 〈 0.01; plasma glucose: 10.2±0.39 versus 8.9±0.41 mmol/l, p 〈 0.025). Pretreatment of rats on a high fat diet causes (1) increased GIP secretion in response to an oral fat load, (2) abolition of the feed-back inhibition of exogenous insulin on fat-stimulated GIP release, and (3) some degree of insulin resistance.
    Type of Medium: Electronic Resource
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