Abstract
The present study examines the effect of concanavalin A (Con A) on the blood insulin and glucose levels of rats. Male and female rats treated with Con A (62.5-500 micrograms/kg) for three days showed a dose- and time-dependent hyperinsulinemia that lasted more than 48 h. Male rats were more sensitive to Con A. Thus, 6 h after treatment with Con A the circulating insulin levels in male rats had increased by 85% (control: 10.2 +/- 0.9 mU/l and Con A-treated: 18.8 +/- 1 mU/l) compared to only 38% (control: 7.5 +/- 0.2 mU/l; Con A-treated: 10.3 +/- mU/l) in females. An identical response was seen after 12 h. Con A (250 micrograms/kg) produced time-dependent hypoglycemia in both sexes but more pronounced in males. There was no correlation between the hypoglycemia and hyperinsulinemia described above. The Con A-induced hyperinsulinemia in rats of both sexes was abolished in gonadectomized animals (intact males: +101 +/- 17% vs orchiectomized males: -5 +/- 3%; intact females: +86 +/- 23% vs ovariectomized females: -18 +/- 7.2%). Pretreating intact male and female rats with human chorionic gonadotropin also significantly inhibited the Con A-induced hyperinsulinemia. Estradiol (10 micrograms/kg,i.m.) significantly blocked the Con A-induced increase in circulating insulin in male rats (101 +/- 17% for controls vs 32 +/- 5.3% for estradiol-treated animals, P < 0.05) while testosterone (10 mg/kg, i.m.) had no similar effect on intact female rats. Pretreating Con A-injected rats with opioid antagonists such as naloxone (1 mg/kg, s.c.) and naltrexone (5 mg/kg, s.c.) blocked the hyperinsulinemia produced by the lectin in males (control: +101 +/- 17% vs naloxone-treated: +5 +/- 14%, or naltrexone-treated: -23 +/- 4.5%) and females (control: +86 +/- 23% vs naloxone-treated: +21 +/- 20%, or naltrexone-treated: -18 +/- 11%). These results demonstrate that Con A increases the levels of circulating insulin in rats and that this response is opioid-dependent and hormonally regulated.
Highlights
Plant lectins are proteins capable of binding to carbohydrates on mammalian cells and membranes
Concanavalin A (Con A) is a glucose/ mannose-binding plant lectin isolated from jack bean (Canavalia ensiformis) seeds that binds extensively to mammalian cell surfaces [10] and exhibits multiplein vitro insulin-like effects [11,12]
Con A and canatoxin (CNTX), a toxic protein isolated from Canavalia ensiformis seeds, are structurally distinct, both substances induce platelet aggregation [19,20], trigger histamine secretion from peritoneal mast cells [21,22,23], and induce paw edema [24,25] and neutrophil chemotaxis in the peritoneal cavity of rats [26,27,28]
Summary
Part of Masters theses presented by J.E. Zambelli and M.H. Pretreating Con A-injected rats with opioid antagonists such as naloxone (1 mg/ kg, sc) and naltrexone (5 mg/kg, sc) blocked the hyperinsulinemia produced by the lectin in males (control: +101 ± 17% vs naloxonetreated: +5 ± 14%, or naltrexone-treated: -23 ± 4.5%) and females (control: +86 ± 23% vs naloxone-treated: +21 ± 20%, or naltrexonetreated: -18 ± 11%). These results demonstrate that Con A increases the levels of circulating insulin in rats and that this response is opioiddependent and hormonally regulated
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