Effect of dietary carbohydrate and phenotype on sucrase, maltase, lactase, and alkaline phosphatase specific activity in SHR/N-cp rat.
The obese spontaneous hypertensive rat/NIH-corpulent (SHR/N-cp) rat exhibits some of the metabolic and pathologic alterations associated with non-insulin-dependent diabetes mellitus and hypertension. The current study was conducted to investigate the influence of phenotype (ob versus In) and source of dietary carbohydrate (sucrose versus starch) on intestinal sucrase, maltase, lactase, and alkaline phosphatase activity in SHR/N-cp rats. For 3 months, lean and obese male SHR/N-cp rats were fed isocaloric diets containing as the sole source of carbohydrate either 54% cooked corn starch or sucrose. Serum and urine markers for diabetes were observed in obese rats. Wet weight and length of intestines were significantly increased in obese rats compared with lean littermates. Among the intestinal enzymes measured, statistical tests confirmed that sucrase activity was significantly increased (P < 0.01) by both phenotype (ob > In) and feeding a sucrose diet. Diet alone (sucrose > starch) significantly increased (P < 0.05) maltase activity in obese rats, but had no effect on lean rats. Lactase activity was significantly higher (P < 0.05) in obese sucrose-fed rats compared with obese starch-fed and/or lean littermates. Statistical tests revealed that intestinal alkaline phosphatase activity was significantly altered (P < 0.05) by both phenotype and diet. Intestinal alkaline phosphatase was higher in starch-fed lean rats compared with lean littermates fed sucrose and to starch or sucrose-fed obese rats. These results are not indicative of a simple, nonspecific increase in intestinal enzyme activity, since the effects observed in intestinal alkaline phosphatase contrast the effects observed in intestinal sucrase, maltase, and lactase activity. These results indicate that both phenotype and diet alter structural and enzymatic intestinal activities of SHR/N-cp rats. Distinct variations in the observed intestinal enzymatic activities suggest that these enzymes are under the control of genetic, hormonal, and dietary factors. Rationale for these differences are discussed.
Wiesenfeld
P
P
Carbohydrate Nutrition Laboratory, Beltsville Human Nutrition Research Center, ARS, U.S. Department of Agriculture, Maryland 20705.
Baldwin
J
J
Szepesi
B
B
Michaelis
O E
OE
D000469:Alkaline Phosphatase / Q000378:metabolism*; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000494:pharmacology*; D006026:Glycoside Hydrolases / Q000378:metabolism*; D006943:Hyperglycemia / Q000209:etiology; D006949:Hyperlipidemias / Q000209:etiology; D006973:Hypertension / Q000235:genetics* / Q000378:metabolism*; D007421:Intestine, Small / Q000033:anatomy & histology / Q000201:enzymology*; D043322:Lactase; D008297:Male; D009765:Obesity / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D013393:Sucrase / Q000378:metabolism; D000520:alpha-Glucosidases / Q000378:metabolism; D001616:beta-Galactosidase / Q000096:biosynthesis
D004040:Dietary Carbohydrates; D000469:Alkaline Phosphatase; D006026:Glycoside Hydrolases; D043322:Lactase; D000520:alpha-Glucosidases; D001616:beta-Galactosidase; D013393:Sucrase