Effect of Dietary Carbohydrate and Phenotype on Sucrase, Maltase, Lactase, and Alkaline Phosphatase Specific Activity in SHR/N-cp Rat
Abstract 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) an...
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| Veröffentlicht in: | Experimental biology and medicine (Maywood, N.J.) N.J.), 1993-03, Vol.202 (3), p.338-344 |
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| creator | Wlesenfeld, P. Baldwin, J. Szepesi, B. Michaelis, O. E. |
| description | Abstract
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 activitywas significantly altered (P < 0.05) by both phenotypeand 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. |
| doi_str_mv | 10.3181/00379727-202-43544 |
| format | Article |
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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 activitywas significantly altered (P < 0.05) by both phenotypeand 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.</description><identifier>ISSN: 0037-9727</identifier><identifier>ISSN: 1535-3702</identifier><identifier>EISSN: 1535-3699</identifier><identifier>EISSN: 1525-1373</identifier><identifier>DOI: 10.3181/00379727-202-43544</identifier><identifier>PMID: 8437990</identifier><identifier>CODEN: PSEBAA</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Alkaline Phosphatase - metabolism ; alpha-Glucosidases - metabolism ; Animals ; beta-Galactosidase - biosynthesis ; Biological and medical sciences ; Diabetes Mellitus, Type 2 - metabolism ; Dietary Carbohydrates - pharmacology ; Glycoside Hydrolases - metabolism ; Hyperglycemia - etiology ; Hyperlipidemias - etiology ; Hypertension - genetics ; Hypertension - metabolism ; Intestine, Small - anatomy & histology ; Intestine, Small - enzymology ; Lactase ; Male ; Medical sciences ; Metabolic diseases ; Obesity ; Obesity - metabolism ; Organ Size ; Rats ; Rats, Inbred SHR ; Sucrase - metabolism</subject><ispartof>Experimental biology and medicine (Maywood, N.J.), 1993-03, Vol.202 (3), p.338-344</ispartof><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-b8a603b0a1069934acbac13149888d832477e37969ea1f3fe6f88d70907290603</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27925,27926</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4643660$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8437990$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wlesenfeld, P.</creatorcontrib><creatorcontrib>Baldwin, J.</creatorcontrib><creatorcontrib>Szepesi, B.</creatorcontrib><creatorcontrib>Michaelis, O. E.</creatorcontrib><title>Effect of Dietary Carbohydrate and Phenotype on Sucrase, Maltase, Lactase, and Alkaline Phosphatase Specific Activity in SHR/N-cp Rat</title><title>Experimental biology and medicine (Maywood, N.J.)</title><addtitle>Proc Soc Exp Biol Med</addtitle><description>Abstract
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 activitywas significantly altered (P < 0.05) by both phenotypeand 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.</description><subject>Alkaline Phosphatase - metabolism</subject><subject>alpha-Glucosidases - metabolism</subject><subject>Animals</subject><subject>beta-Galactosidase - biosynthesis</subject><subject>Biological and medical sciences</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Dietary Carbohydrates - pharmacology</subject><subject>Glycoside Hydrolases - metabolism</subject><subject>Hyperglycemia - etiology</subject><subject>Hyperlipidemias - etiology</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Intestine, Small - anatomy & histology</subject><subject>Intestine, Small - enzymology</subject><subject>Lactase</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Obesity</subject><subject>Obesity - metabolism</subject><subject>Organ Size</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Sucrase - metabolism</subject><issn>0037-9727</issn><issn>1535-3702</issn><issn>1535-3699</issn><issn>1525-1373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMuO0zAUhi0EGsrACyAheYFYEWrHTpwsqzIwSOWiGVhbJ-4x9ZDGGdtB6gPw3jhtmSUrH_m_2Ocj5CVn7wRv-JIxoVpVqqJkZSFFJeUjsuCVqApRt-1jspgNxex4Sp7FeMcYr1RZX5CLRuZkyxbkz5W1aBL1lr53mCAc6BpC53eHbYCEFIYt_bbDwafDiNQP9HYyASK-pZ-hT8dhA-Y0zN5V_wt6N2AO-TjuYFbo7YjGWWfoyiT326UDdbno-mb5pTAjvYH0nDyx0Ed8cT4vyY8PV9_X18Xm68dP69WmMFKIVHQN1Ex0DDjL-wkJpgPDBZdt0zTbRpRSKcyL1S0Ct8JibfO9Yi1TZcty9JK8OfWOwd9PGJPeu2iw72FAP0WtqipXiSYby5PRBB9jQKvH4PaZjuZMz-z1P_Y6s9dH9jn06tw-dXvcPkTOsLP--qxDNNDbAINx8cEmaynq4yeXJ1uEn6jv_BSGzOR_D_8Fn3SYFA</recordid><startdate>19930301</startdate><enddate>19930301</enddate><creator>Wlesenfeld, P.</creator><creator>Baldwin, J.</creator><creator>Szepesi, B.</creator><creator>Michaelis, O. E.</creator><general>SAGE Publications</general><general>Blackwell Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19930301</creationdate><title>Effect of Dietary Carbohydrate and Phenotype on Sucrase, Maltase, Lactase, and Alkaline Phosphatase Specific Activity in SHR/N-cp Rat</title><author>Wlesenfeld, P. ; Baldwin, J. ; Szepesi, B. ; Michaelis, O. E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-b8a603b0a1069934acbac13149888d832477e37969ea1f3fe6f88d70907290603</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Alkaline Phosphatase - metabolism</topic><topic>alpha-Glucosidases - metabolism</topic><topic>Animals</topic><topic>beta-Galactosidase - biosynthesis</topic><topic>Biological and medical sciences</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Dietary Carbohydrates - pharmacology</topic><topic>Glycoside Hydrolases - metabolism</topic><topic>Hyperglycemia - etiology</topic><topic>Hyperlipidemias - etiology</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Intestine, Small - anatomy & histology</topic><topic>Intestine, Small - enzymology</topic><topic>Lactase</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Obesity</topic><topic>Obesity - metabolism</topic><topic>Organ Size</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Sucrase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wlesenfeld, P.</creatorcontrib><creatorcontrib>Baldwin, J.</creatorcontrib><creatorcontrib>Szepesi, B.</creatorcontrib><creatorcontrib>Michaelis, O. E.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental biology and medicine (Maywood, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wlesenfeld, P.</au><au>Baldwin, J.</au><au>Szepesi, B.</au><au>Michaelis, O. E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Dietary Carbohydrate and Phenotype on Sucrase, Maltase, Lactase, and Alkaline Phosphatase Specific Activity in SHR/N-cp Rat</atitle><jtitle>Experimental biology and medicine (Maywood, N.J.)</jtitle><addtitle>Proc Soc Exp Biol Med</addtitle><date>1993-03-01</date><risdate>1993</risdate><volume>202</volume><issue>3</issue><spage>338</spage><epage>344</epage><pages>338-344</pages><issn>0037-9727</issn><issn>1535-3702</issn><eissn>1535-3699</eissn><eissn>1525-1373</eissn><coden>PSEBAA</coden><abstract>Abstract
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 activitywas significantly altered (P < 0.05) by both phenotypeand 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.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>8437990</pmid><doi>10.3181/00379727-202-43544</doi><tpages>7</tpages></addata></record> |
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| ispartof | Experimental biology and medicine (Maywood, N.J.), 1993-03, Vol.202 (3), p.338-344 |
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| subjects | Alkaline Phosphatase - metabolism alpha-Glucosidases - metabolism Animals beta-Galactosidase - biosynthesis Biological and medical sciences Diabetes Mellitus, Type 2 - metabolism Dietary Carbohydrates - pharmacology Glycoside Hydrolases - metabolism Hyperglycemia - etiology Hyperlipidemias - etiology Hypertension - genetics Hypertension - metabolism Intestine, Small - anatomy & histology Intestine, Small - enzymology Lactase Male Medical sciences Metabolic diseases Obesity Obesity - metabolism Organ Size Rats Rats, Inbred SHR Sucrase - metabolism |
| title | Effect of Dietary Carbohydrate and Phenotype on Sucrase, Maltase, Lactase, and Alkaline Phosphatase Specific Activity in SHR/N-cp Rat |
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