Sulfonyl(thio)urea derivative induction of insulin secretion is mediated by potassium, calcium, and sodium channel signal transduction
Aim To investigate the mechanism of action of sulfonyl(thio)urea derivative (SD) on glycemia and on insulin secretion in pancreatic islets. Methods Wistar rats were divided into hyperglycemic control group, rats received 4 g/kg body weight glucose plus sitagliptin 10 mg/kg (p.o.); hyperglycemic plus...
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| Veröffentlicht in: | Journal of cellular physiology 2019-07, Vol.234 (7), p.10138-10147 |
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| creator | Sulis, Paola Miranda Dambrós, Betina Fernanda Mascarello, Alessandra dos Santos, Adair Roberto Soares Yunes, Rosendo Augusto Nunes, Ricardo José Frederico, Marisa Jádna Silva Barreto Silva, Fátima Regina Mena |
| description | Aim
To investigate the mechanism of action of sulfonyl(thio)urea derivative (SD) on glycemia and on insulin secretion in pancreatic islets.
Methods
Wistar rats were divided into hyperglycemic control group, rats received 4 g/kg body weight glucose plus sitagliptin 10 mg/kg (p.o.); hyperglycemic plus SD 10 mg/kg (p.o.); hyperglycemic plus SD plus sitagliptin. Blood was collected before glucose overloading (zero time), and at 15, 30, 60, and 180 min after glucose, from the afore mentioned groups for glycemia and glucagon‐like peptide 1 (GLP‐1) measurements and intestinal disaccharidases activity. Pancreatic islets were isolated for the calcium influx and insulin secretion in in vitro studies.
Results
SD reduced glycemia and increased GLP‐1 secretion, while inhibited sucrase and lactase activity. This SD (1.0 and 10.0 µM) stimulated calcium influx in a similar percentile to that of glibenclamide, and in a nonsynergic manner. In addition, the trigger effect of SD on calcium influx was through the K+‐ATP‐dependent channels, and partially by activating voltage‐dependent K
+ channels and voltage‐dependent calcium channels. Furthermore, SD‐stimulated Na
+ and Ca
2+ entry, induced by the transient receptor potential ankyrin 1 and by modulation of Na
+/Ca
2+ exchange. The activation of these pathways by SD culminated in in vitro insulin secretion, reinforcing the critical role of K
+‐ATP channels in the secretagogue effect of SD.
Conclusions
SD diminish glycemia by inducing GLP‐1 secretion and inhibiting disaccharidases. To our knowledge, this is the first report of an insulin secretagogue effect of SD that is mediated by potassium and calcium, as well as sodium, signal transduction.
Sulfonyl(thio)urea derivative (SD) stimulates insulin secretion. Mechanism of action of SD on insulin secretion is mediated by potassium, calcium, and sodium. |
| doi_str_mv | 10.1002/jcp.27680 |
| format | Article |
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To investigate the mechanism of action of sulfonyl(thio)urea derivative (SD) on glycemia and on insulin secretion in pancreatic islets.
Methods
Wistar rats were divided into hyperglycemic control group, rats received 4 g/kg body weight glucose plus sitagliptin 10 mg/kg (p.o.); hyperglycemic plus SD 10 mg/kg (p.o.); hyperglycemic plus SD plus sitagliptin. Blood was collected before glucose overloading (zero time), and at 15, 30, 60, and 180 min after glucose, from the afore mentioned groups for glycemia and glucagon‐like peptide 1 (GLP‐1) measurements and intestinal disaccharidases activity. Pancreatic islets were isolated for the calcium influx and insulin secretion in in vitro studies.
Results
SD reduced glycemia and increased GLP‐1 secretion, while inhibited sucrase and lactase activity. This SD (1.0 and 10.0 µM) stimulated calcium influx in a similar percentile to that of glibenclamide, and in a nonsynergic manner. In addition, the trigger effect of SD on calcium influx was through the K+‐ATP‐dependent channels, and partially by activating voltage‐dependent K
+ channels and voltage‐dependent calcium channels. Furthermore, SD‐stimulated Na
+ and Ca
2+ entry, induced by the transient receptor potential ankyrin 1 and by modulation of Na
+/Ca
2+ exchange. The activation of these pathways by SD culminated in in vitro insulin secretion, reinforcing the critical role of K
+‐ATP channels in the secretagogue effect of SD.
Conclusions
SD diminish glycemia by inducing GLP‐1 secretion and inhibiting disaccharidases. To our knowledge, this is the first report of an insulin secretagogue effect of SD that is mediated by potassium and calcium, as well as sodium, signal transduction.
Sulfonyl(thio)urea derivative (SD) stimulates insulin secretion. Mechanism of action of SD on insulin secretion is mediated by potassium, calcium, and sodium.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.27680</identifier><identifier>PMID: 30417369</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Animals ; Ankyrins ; ATP ; Blood glucose ; Body weight ; Calcium channels ; Calcium channels (voltage-gated) ; Calcium Channels - drug effects ; Calcium Channels - metabolism ; Calcium influx ; Calcium ions ; Calcium signalling ; Channels ; Electric potential ; Glibenclamide ; Glucagon ; Glucagon-Like Peptide 1 - metabolism ; Glucose ; Hyperglycemia - metabolism ; Hypoglycemic Agents - pharmacology ; Insulin ; insulin secretagogue ; Insulin secretion ; Insulin Secretion - drug effects ; Intestine ; Islets of Langerhans - drug effects ; Islets of Langerhans - metabolism ; Lactase ; Male ; Overloading ; Pancreas ; Potassium ; potassium channels ; Potassium channels (voltage-gated) ; Potassium Channels, Voltage-Gated - drug effects ; Potassium Channels, Voltage-Gated - metabolism ; Rats ; Rats, Wistar ; Rodents ; Secretion ; Signal transduction ; Signal Transduction - drug effects ; Sitagliptin Phosphate - pharmacology ; Sodium ; sodium channels ; sulfonyl(thio)urea ; Sulfonylurea Compounds - pharmacology ; Transient receptor potential proteins ; Urea ; VDCC ; Voltage-Gated Sodium Channels - drug effects ; Voltage-Gated Sodium Channels - metabolism</subject><ispartof>Journal of cellular physiology, 2019-07, Vol.234 (7), p.10138-10147</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><rights>2019 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-dd9c4f86a828bd641e15e4f33d96107d1597963b8d7d4efbdb2819fa7b1f28e43</citedby><cites>FETCH-LOGICAL-c3530-dd9c4f86a828bd641e15e4f33d96107d1597963b8d7d4efbdb2819fa7b1f28e43</cites><orcidid>0000-0002-1391-2354</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.27680$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.27680$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30417369$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sulis, Paola Miranda</creatorcontrib><creatorcontrib>Dambrós, Betina Fernanda</creatorcontrib><creatorcontrib>Mascarello, Alessandra</creatorcontrib><creatorcontrib>dos Santos, Adair Roberto Soares</creatorcontrib><creatorcontrib>Yunes, Rosendo Augusto</creatorcontrib><creatorcontrib>Nunes, Ricardo José</creatorcontrib><creatorcontrib>Frederico, Marisa Jádna Silva</creatorcontrib><creatorcontrib>Barreto Silva, Fátima Regina Mena</creatorcontrib><title>Sulfonyl(thio)urea derivative induction of insulin secretion is mediated by potassium, calcium, and sodium channel signal transduction</title><title>Journal of cellular physiology</title><addtitle>J Cell Physiol</addtitle><description>Aim
To investigate the mechanism of action of sulfonyl(thio)urea derivative (SD) on glycemia and on insulin secretion in pancreatic islets.
Methods
Wistar rats were divided into hyperglycemic control group, rats received 4 g/kg body weight glucose plus sitagliptin 10 mg/kg (p.o.); hyperglycemic plus SD 10 mg/kg (p.o.); hyperglycemic plus SD plus sitagliptin. Blood was collected before glucose overloading (zero time), and at 15, 30, 60, and 180 min after glucose, from the afore mentioned groups for glycemia and glucagon‐like peptide 1 (GLP‐1) measurements and intestinal disaccharidases activity. Pancreatic islets were isolated for the calcium influx and insulin secretion in in vitro studies.
Results
SD reduced glycemia and increased GLP‐1 secretion, while inhibited sucrase and lactase activity. This SD (1.0 and 10.0 µM) stimulated calcium influx in a similar percentile to that of glibenclamide, and in a nonsynergic manner. In addition, the trigger effect of SD on calcium influx was through the K+‐ATP‐dependent channels, and partially by activating voltage‐dependent K
+ channels and voltage‐dependent calcium channels. Furthermore, SD‐stimulated Na
+ and Ca
2+ entry, induced by the transient receptor potential ankyrin 1 and by modulation of Na
+/Ca
2+ exchange. The activation of these pathways by SD culminated in in vitro insulin secretion, reinforcing the critical role of K
+‐ATP channels in the secretagogue effect of SD.
Conclusions
SD diminish glycemia by inducing GLP‐1 secretion and inhibiting disaccharidases. To our knowledge, this is the first report of an insulin secretagogue effect of SD that is mediated by potassium and calcium, as well as sodium, signal transduction.
Sulfonyl(thio)urea derivative (SD) stimulates insulin secretion. Mechanism of action of SD on insulin secretion is mediated by potassium, calcium, and sodium.</description><subject>Animals</subject><subject>Ankyrins</subject><subject>ATP</subject><subject>Blood glucose</subject><subject>Body weight</subject><subject>Calcium channels</subject><subject>Calcium channels (voltage-gated)</subject><subject>Calcium Channels - drug effects</subject><subject>Calcium Channels - metabolism</subject><subject>Calcium influx</subject><subject>Calcium ions</subject><subject>Calcium signalling</subject><subject>Channels</subject><subject>Electric potential</subject><subject>Glibenclamide</subject><subject>Glucagon</subject><subject>Glucagon-Like Peptide 1 - metabolism</subject><subject>Glucose</subject><subject>Hyperglycemia - metabolism</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Insulin</subject><subject>insulin secretagogue</subject><subject>Insulin secretion</subject><subject>Insulin Secretion - drug effects</subject><subject>Intestine</subject><subject>Islets of Langerhans - drug effects</subject><subject>Islets of Langerhans - metabolism</subject><subject>Lactase</subject><subject>Male</subject><subject>Overloading</subject><subject>Pancreas</subject><subject>Potassium</subject><subject>potassium channels</subject><subject>Potassium channels (voltage-gated)</subject><subject>Potassium Channels, Voltage-Gated - drug effects</subject><subject>Potassium Channels, Voltage-Gated - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Secretion</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Sitagliptin Phosphate - pharmacology</subject><subject>Sodium</subject><subject>sodium channels</subject><subject>sulfonyl(thio)urea</subject><subject>Sulfonylurea Compounds - pharmacology</subject><subject>Transient receptor potential proteins</subject><subject>Urea</subject><subject>VDCC</subject><subject>Voltage-Gated Sodium Channels - drug effects</subject><subject>Voltage-Gated Sodium Channels - metabolism</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kdtKXDEUhkOx1NH2oi9QAt4ouDWHfcqlDNYDgkLb6012slIzZJJpsqPMC_jcjTNTL4RerbWSj4_F-hH6SskZJYSdL9TqjHVtTz6gGSWiq-q2YXtoVv5oJZqa7qODlBaEECE4_4T2Oalpx1sxQy8_sjPBr93x9GjDSY4gsYZon-RknwBbr7OabPA4mDKk7KzHCVSEzaNNeAnaygk0Htd4FSaZks3LU6ykU5tGeo1T0KXH6lF6Dw4n-9tLh6cofdrpP6OPRroEX3b1EP36fvlzfl3d3V_dzC_uKsUbTiqthapN38qe9aNuawq0gdpwrkVLSadpIzrR8rHXna7BjHpkPRVGdiM1rIeaH6LjrXcVw58MaRqWNilwTnoIOQ2McsYaQRgv6NE7dBFyLIu_UuWMhPOWFOpkS6kYUopghlW0SxnXAyXDazhDCWfYhFPYbztjHsvZ3sh_aRTgfAs8Wwfr_5uG2_nDVvkX03Oa1w</recordid><startdate>201907</startdate><enddate>201907</enddate><creator>Sulis, Paola Miranda</creator><creator>Dambrós, Betina Fernanda</creator><creator>Mascarello, Alessandra</creator><creator>dos Santos, Adair Roberto Soares</creator><creator>Yunes, Rosendo Augusto</creator><creator>Nunes, Ricardo José</creator><creator>Frederico, Marisa Jádna Silva</creator><creator>Barreto Silva, Fátima Regina Mena</creator><general>Wiley Subscription Services, Inc</general><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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1391-2354</orcidid></search><sort><creationdate>201907</creationdate><title>Sulfonyl(thio)urea derivative induction of insulin secretion is mediated by potassium, calcium, and sodium channel signal transduction</title><author>Sulis, Paola Miranda ; Dambrós, Betina Fernanda ; Mascarello, Alessandra ; dos Santos, Adair Roberto Soares ; Yunes, Rosendo Augusto ; Nunes, Ricardo José ; Frederico, Marisa Jádna Silva ; Barreto Silva, Fátima Regina Mena</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-dd9c4f86a828bd641e15e4f33d96107d1597963b8d7d4efbdb2819fa7b1f28e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Ankyrins</topic><topic>ATP</topic><topic>Blood glucose</topic><topic>Body weight</topic><topic>Calcium channels</topic><topic>Calcium channels (voltage-gated)</topic><topic>Calcium Channels - drug effects</topic><topic>Calcium Channels - metabolism</topic><topic>Calcium influx</topic><topic>Calcium ions</topic><topic>Calcium signalling</topic><topic>Channels</topic><topic>Electric potential</topic><topic>Glibenclamide</topic><topic>Glucagon</topic><topic>Glucagon-Like Peptide 1 - metabolism</topic><topic>Glucose</topic><topic>Hyperglycemia - metabolism</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Insulin</topic><topic>insulin secretagogue</topic><topic>Insulin secretion</topic><topic>Insulin Secretion - drug effects</topic><topic>Intestine</topic><topic>Islets of Langerhans - drug effects</topic><topic>Islets of Langerhans - metabolism</topic><topic>Lactase</topic><topic>Male</topic><topic>Overloading</topic><topic>Pancreas</topic><topic>Potassium</topic><topic>potassium channels</topic><topic>Potassium channels (voltage-gated)</topic><topic>Potassium Channels, Voltage-Gated - drug effects</topic><topic>Potassium Channels, Voltage-Gated - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Secretion</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Sitagliptin Phosphate - pharmacology</topic><topic>Sodium</topic><topic>sodium channels</topic><topic>sulfonyl(thio)urea</topic><topic>Sulfonylurea Compounds - pharmacology</topic><topic>Transient receptor potential proteins</topic><topic>Urea</topic><topic>VDCC</topic><topic>Voltage-Gated Sodium Channels - drug effects</topic><topic>Voltage-Gated Sodium Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sulis, Paola Miranda</creatorcontrib><creatorcontrib>Dambrós, Betina Fernanda</creatorcontrib><creatorcontrib>Mascarello, Alessandra</creatorcontrib><creatorcontrib>dos Santos, Adair Roberto Soares</creatorcontrib><creatorcontrib>Yunes, Rosendo Augusto</creatorcontrib><creatorcontrib>Nunes, Ricardo José</creatorcontrib><creatorcontrib>Frederico, Marisa Jádna Silva</creatorcontrib><creatorcontrib>Barreto Silva, Fátima Regina Mena</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sulis, Paola Miranda</au><au>Dambrós, Betina Fernanda</au><au>Mascarello, Alessandra</au><au>dos Santos, Adair Roberto Soares</au><au>Yunes, Rosendo Augusto</au><au>Nunes, Ricardo José</au><au>Frederico, Marisa Jádna Silva</au><au>Barreto Silva, Fátima Regina Mena</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sulfonyl(thio)urea derivative induction of insulin secretion is mediated by potassium, calcium, and sodium channel signal transduction</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J Cell Physiol</addtitle><date>2019-07</date><risdate>2019</risdate><volume>234</volume><issue>7</issue><spage>10138</spage><epage>10147</epage><pages>10138-10147</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>Aim
To investigate the mechanism of action of sulfonyl(thio)urea derivative (SD) on glycemia and on insulin secretion in pancreatic islets.
Methods
Wistar rats were divided into hyperglycemic control group, rats received 4 g/kg body weight glucose plus sitagliptin 10 mg/kg (p.o.); hyperglycemic plus SD 10 mg/kg (p.o.); hyperglycemic plus SD plus sitagliptin. Blood was collected before glucose overloading (zero time), and at 15, 30, 60, and 180 min after glucose, from the afore mentioned groups for glycemia and glucagon‐like peptide 1 (GLP‐1) measurements and intestinal disaccharidases activity. Pancreatic islets were isolated for the calcium influx and insulin secretion in in vitro studies.
Results
SD reduced glycemia and increased GLP‐1 secretion, while inhibited sucrase and lactase activity. This SD (1.0 and 10.0 µM) stimulated calcium influx in a similar percentile to that of glibenclamide, and in a nonsynergic manner. In addition, the trigger effect of SD on calcium influx was through the K+‐ATP‐dependent channels, and partially by activating voltage‐dependent K
+ channels and voltage‐dependent calcium channels. Furthermore, SD‐stimulated Na
+ and Ca
2+ entry, induced by the transient receptor potential ankyrin 1 and by modulation of Na
+/Ca
2+ exchange. The activation of these pathways by SD culminated in in vitro insulin secretion, reinforcing the critical role of K
+‐ATP channels in the secretagogue effect of SD.
Conclusions
SD diminish glycemia by inducing GLP‐1 secretion and inhibiting disaccharidases. To our knowledge, this is the first report of an insulin secretagogue effect of SD that is mediated by potassium and calcium, as well as sodium, signal transduction.
Sulfonyl(thio)urea derivative (SD) stimulates insulin secretion. Mechanism of action of SD on insulin secretion is mediated by potassium, calcium, and sodium.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30417369</pmid><doi>10.1002/jcp.27680</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-1391-2354</orcidid></addata></record> |
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| ispartof | Journal of cellular physiology, 2019-07, Vol.234 (7), p.10138-10147 |
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| subjects | Animals Ankyrins ATP Blood glucose Body weight Calcium channels Calcium channels (voltage-gated) Calcium Channels - drug effects Calcium Channels - metabolism Calcium influx Calcium ions Calcium signalling Channels Electric potential Glibenclamide Glucagon Glucagon-Like Peptide 1 - metabolism Glucose Hyperglycemia - metabolism Hypoglycemic Agents - pharmacology Insulin insulin secretagogue Insulin secretion Insulin Secretion - drug effects Intestine Islets of Langerhans - drug effects Islets of Langerhans - metabolism Lactase Male Overloading Pancreas Potassium potassium channels Potassium channels (voltage-gated) Potassium Channels, Voltage-Gated - drug effects Potassium Channels, Voltage-Gated - metabolism Rats Rats, Wistar Rodents Secretion Signal transduction Signal Transduction - drug effects Sitagliptin Phosphate - pharmacology Sodium sodium channels sulfonyl(thio)urea Sulfonylurea Compounds - pharmacology Transient receptor potential proteins Urea VDCC Voltage-Gated Sodium Channels - drug effects Voltage-Gated Sodium Channels - metabolism |
| title | Sulfonyl(thio)urea derivative induction of insulin secretion is mediated by potassium, calcium, and sodium channel signal transduction |
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