Abstract：Objective To study the effects of embryonic lead exposure on food intake and bowel movement in offspring rats and possible mechanisms. Methods Sprague-Dawley rats were given 0.1% (low-dose lead exposure group) or 0.2% (high-dose lead exposure group) lead acetate freely during pregnancy to establish an animal model of embryonic lead exposure. A blank control group was also established. The male offspring rats were enrolled in the study, and 10 male offspring rats from each group were selected to observe the changes in food intake, bowel movement, gastric emptying, intestine propulsion, and pathological inflammatory response in the gastric mucosa. Eight offspring rats were selected from each group, and electron microscopy and immunohistochemistry were used to observe the changes in the ultrastructure of jejunal microvilli and cell junction and the expression of cholecystokinin-8 (CCK-8) and motilin (MTL) in the feeding center, in order to reveal the possible mechanisms for abnormal gastrointestinal motility in offspring rats induced by embryonic lead exposure. Results Compared with the control group, the low- and high-dose lead exposure groups had a significant reduction in daily food intake, a significant increase in water content of feces, a significant reduction in fecal pellet weight, and a significant increase in small intestine propulsion (P < 0.05). The highdose lead exposure group had a significant reduction in gastric emptying ability compared with the control group (P < 0.05). Compared with the control group, the lead exposure groups had significantly greater pathological inflammatory changes in the gastric mucosa (P < 0.05), significant reductions in the number and length of the jejunal microvilli and the number of epithelial desmosome junctions (P < 0.05), a significant increase in the macula densa gap (P < 0.05), and significant increases in the expression of MTL and CCK-8 in the feeding center (P < 0.05), in a dose-dependent manner. Conclusions The degree of gastrointestinal structural injury and expression levels of MTL and CCK-8 in the feeding center are lead dose-dependent, which may be important mechanisms for changes in food intake, bowel movement, and digestive functions in offspring rats induced by embryonic lead exposure.
ZHOU Jian-Ping,WANG Fan,YI Xiao-Qing et al. Effects of embryonic lead exposure on food intake and bowel movement in offspring rats and possible mechanisms[J]. CJCP, 2017, 19(4): 463-469.
Assi MA, Hezmee MN, Haron AW, et al. The detrimental effects of lead on human and animal health[J]. Vet World, 2016, 9(6):660-671.
[2]
Mongolu S, Sharp P. Acute abdominal pain and constipation due to lead poisoning[J]. Acute Med, 2013, 12(4):224-226.
[3]
Vossoughinia H, Pourakbar A, Esfandiari S, et al. Severe abdominal pain caused by lead toxicity without response to oral chelators:a case report[J]. Middle East J Dig Dis, 2016, 8(1):67-72.
[4]
Rosner D. A lead poisoning crisis enters its second century[J]. Health Aff (Millwood), 2016, 35(5):756-759.
[5]
Alba A, Carleton L, Dinkel L, et al. Increased lead levels in pregnancy among immigrant women[J]. J Midwifery Womens Health, 2012, 57(5):509-514.
[6]
Mazumdar I, Goswami K. Congenital lead poisoning:an unusual presentation[J]. Indian J Clin Biochem, 2014, 29(2):257-259.
Zhang ZH, Qin CK, Wu SD, et al. Roles of sphincter of Oddi motility and serum vasoactive intestinal peptide, gastrin and cholecystokinin octapeptide[J]. World J Gastroenterol, 2014, 20(16):4730-4736.
[15]
Alén F, Ramírez-López MT, Gómez de Heras R, et al. Cannabinoid receptors and cholecystokinin in feeding inhibition[J]. Vitam Horm, 2013, 92:165-196.
[16]
Sobrino Crespo C, Perianes Cachero A, Puebla Jiménez L. Peptides and food intake[J]. Front Endocrinol (Lausanne), 2014, 5:58.
Gamble J, Kenny S, Dockray GJ. Plasminogen activator inhibitor (PAI)-1 suppresses inhibition of gastric emptying by cholecystokinin (CCK) in mice[J]. Regul Pept, 2013, 185:9-13.
[19]
Blevins JE, Stanley BG, Reidelberger RD. Brain regions where cholecystokinin suppresses feeding in rats[J]. Brain Res, 2000, 860(1-2):1-10.
[20]
Staljanssens D, Azari EK, Christiaens O, et al. The CCK (-like) receptor in the animal kingdom:functions, evolution and structures[J]. Peptides, 2011, 32(3):607-619.
[21]
Stengel A, Taché Y. Interaction between gastric and upper small intestinal hormones in the regulation of hunger and satiety:ghrelin and cholecystokinin take the central stage[J]. Curr Protein Pept Sci, 2011, 12(4):293-304.
[22]
Dockray GJ. Gastrointestinal hormones and the dialogue between gut and brain[J]. J Physiol, 2014, 592(14):2927-2941.
[23]
Mondal A, Xie Z, Miyano Y, et al. Coordination of motilin and ghrelin regulates the migrating motor complex of gastrointestinal motility in Suncus murinus[J]. Am J Physiol Gastrointest Liver Physiol, 2012, 302(10):G1207-G1215.
