Dietary kidney bean lectins affect insulin levels, change gene expression and modulate metabolism
At high dietary concentrations kidney bean lectins severely impair the growth and health of animals by causing alterations both in local (gut) and systemic metabolism. This results in a switch to a catabolic state and to great loss of body reserves of lipid, glycogen and muscle protein. In the present work the potential role of hormones, in particular, insulin, in mediating some of the toxic effects of dietary kidney bean lectin was studied. The overall results indicated that: (a) Short- or long-term dietary exposure to kidney bean caused a severe reduction in circulating insulin concentration in Hooded-Lister rats and this effect was primarily due to a direct action of the constituent lectins. (b) PHA-E3L depressed blood insulin levels not only when fed to rats continuously for 3-10 days, but also on a single first exposure to the isolectin. In contrast, with PHA-L4 the animals required pre-exposure to this isolectin for several days before it had significant effect on blood insulin levels. (c) PHA appeared to reduce circulating insulin levels initially by interfering with its secretion from the pancreas. At later stages both insulin synthesis and secretion were impaired. (d) Normal blood glucose concentrations were maintained in rats fed with kidney bean lectins despite the low circulating insulin levels. This suggested that in order to maintain euglycaemia the production/or secretion of other hormones involved in regulating glycaemia may also have been altered. (e) Chronic exposure to dietary PHA caused differential changes in insulin receptor and glucose transporter (Glut-4) mRNAs expression leading to an increase in the number of insulin receptors and Glut-4 on skeletal muscle. This up-regulation may increase the insulin sensitivity of the tissue and this may be one of the metabolic factors regulating glucose homeostasis in kidney bean-fed animals. (f) Dietary kidney beans could be utilised to depress circulating insulin levels in the genetically obese hyperinsulinaemic Zucker rat whilst maintaining euglycaemia. However, unlike the findings with the normal Hooded-Lister rats in which dietary PHA was found to impair both insulin synthesis and secretion, in the obese Zucker rat the dietary lectin apparently reduced circulating insulin levels in the short term by interfering only with its secretion by the pancreas. It is thus likely that some of the toxic effects of dietary kidney bean lectins are hormonally mediated and due, at least in part, to impairment of pancreatic insulin production by the lectin.