Normal pancreatic and intestinal enzymes in hypophagic growth-retarded rats that received dorsomedial hypothalamic lesions shortly after weaning

Abstract

Male weanling Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic nuclei (DMNL rats). Sham-operated rats served as controls. After being fed lab chow for two postoperative weeks, the animals were divided into four groups. One group of DMNL rats and controls received a high-caloric diet (high-fat diet, chocolate chip cookies, 32% sucrose solution, potato chips and marshmallows), whereas another group of DMNL rats and controls continued to receive lab chow. The experiment was terminated on the 185th postoperative day. In accordance with previous findings, DMNL rats, irrespective of diet, were lighter and shorter than controls. In addition, DMNL rats fed junk food were lighter than DMNL rats fed lab chow, and junk-fed controls weighed as much as chow-fed controls. Both DMNL rats and controls fed junk food were also shorter and showed higher carcass fat than their chow-fed counterparts. Also, DMNL rats fed junk food had less carcass fat than junk-fed sham-operated controls, whereas in accordance with previous findings, there was no difference between chow-fed DMNL rats and chow-fed sham-operated controls. Irrespective of diet, DMNL rats ate less calories than their respective sham-operated controls. Both absolute and percent pancreas weight and protein pancreas weight and protein/pancreas were unaffected in DMNL rate but were reduced in both junk-fed groups in comparison with their chow-fed counterparts. Both concentrations and contents of pancreatic trypsinogen, amylase and lipase were unaffected in DMNL rats but total activities of all three enzymes were dramatically reduced in the junk-fed compared with the chow-fed DMNL rats. Total activities of trypsinogen and amylase but not lipase were also reduced. Duodenal mucosal weight, total protein and specific activities of enterokinase, leucine amino peptidase and maltase were uninfluenced by lesions and diet alike. In the jejunum, specific activity of enterokinase was dramatically reduced in junk-fed versus chow-fed DMNL rats; the same obtained for junk-fed vs. chow-fed sham-operated control groups. Jejunal lactase, sucrose and maltase were not affected by DMN lesions but both DMNL rats and sham-operated controls fed junk foods showed lower specific activities than their chow-fed counterparts. The data indicate that production of DMN lesions in weanling rats, although followed by dramatic alterations in ponderal and linear growth and food intake, causes little, if any, changes in a number of pancreatic and small intestinal parameters, including enzymes. The only significant changes are those related to diet effects. These findings suggest that the DMNL rat responds to dietary factors like its sham-operated control and suggest that changes in digestive function cannot be invoked as possible causes of growth retardation and food intake in the weanling DMNL rat.