Changes in Refraction Caused by Induction of Acute Hyperglycemia in Healthy Volunteers
Purpose: To determine whether the myopic changes and ocular hypotension after a glucose load are caused by hyperglycemia. Methods: Oral glucose tolerance tests were conducted on seven healthy young subjects with normal vision. The changes in the hematologic parameters and the refractive system were...
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| Veröffentlicht in: | Japanese journal of ophthalmology 1999-09, Vol.43 (5), p.398-403 |
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| creator | Furushima, Masatoshi Imaizumi, Masamoto Nakatsuka, Kazuo |
| description | Purpose: To determine whether the myopic changes and ocular hypotension after a glucose load are caused by hyperglycemia.
Methods: Oral glucose tolerance tests were conducted on seven healthy young subjects with normal vision. The changes in the hematologic parameters and the refractive system were measured periodically for 150 minutes after the glucose load.
Results: After the glucose load, there was an increase in plasma glucose level and the level of plasma osmosis, ocular hypotension, a myopic change in refractive power, shallowing of the anterior chamber, and a thickening of the lens. The degree of the myopic change exceeded the power of the residual accommodation. Normalization of the plasma glucose level led to a normalization of the intraocular pressure and a reversal of the myopic changes.
Conclusions: These findings suggest that the myopic changes that accompanied hyperglycemia were caused by a thickening of the lens resulting from a decrease in the tension of the zonule fibers of Zinn, and were secondary to ocular hypotension. Hyperopia appeared to be caused by the reversal of the myopia after normalization of plasma glucose levels. |
| doi_str_mv | 10.1016/S0021-5155(99)00098-2 |
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Methods: Oral glucose tolerance tests were conducted on seven healthy young subjects with normal vision. The changes in the hematologic parameters and the refractive system were measured periodically for 150 minutes after the glucose load.
Results: After the glucose load, there was an increase in plasma glucose level and the level of plasma osmosis, ocular hypotension, a myopic change in refractive power, shallowing of the anterior chamber, and a thickening of the lens. The degree of the myopic change exceeded the power of the residual accommodation. Normalization of the plasma glucose level led to a normalization of the intraocular pressure and a reversal of the myopic changes.
Conclusions: These findings suggest that the myopic changes that accompanied hyperglycemia were caused by a thickening of the lens resulting from a decrease in the tension of the zonule fibers of Zinn, and were secondary to ocular hypotension. Hyperopia appeared to be caused by the reversal of the myopia after normalization of plasma glucose levels.</description><identifier>ISSN: 0021-5155</identifier><identifier>EISSN: 1613-2246</identifier><identifier>DOI: 10.1016/S0021-5155(99)00098-2</identifier><identifier>PMID: 10580662</identifier><identifier>CODEN: JJOPA7</identifier><language>eng</language><publisher>Heidelberg: Elsevier Inc</publisher><subject>Accommodation, Ocular ; Acute Disease ; Administration, Oral ; Adolescent ; Adult ; Biological and medical sciences ; Blood Glucose - metabolism ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Glucose - administration & dosage ; Glucose load ; Glucose Tolerance Test ; Humans ; hyperglycemia ; Hyperglycemia - blood ; Hyperglycemia - complications ; Hyperglycemia - physiopathology ; Insulin - blood ; Intraocular Pressure ; IOP ; lens ; Lens, Crystalline - physiopathology ; Ligaments - physiopathology ; Male ; Medical sciences ; myopia ; Myopia - blood ; Myopia - etiology ; Myopia - physiopathology ; Ocular Hypotension - blood ; Ocular Hypotension - etiology ; Ocular Hypotension - physiopathology ; Somatostatin - administration & dosage</subject><ispartof>Japanese journal of ophthalmology, 1999-09, Vol.43 (5), p.398-403</ispartof><rights>1999 Japanese Ophthalmological Society</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-ec271658b19fa296e79d721b87a529471ba1141a3e8a83d45a7fae446401b6383</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1984006$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10580662$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Furushima, Masatoshi</creatorcontrib><creatorcontrib>Imaizumi, Masamoto</creatorcontrib><creatorcontrib>Nakatsuka, Kazuo</creatorcontrib><title>Changes in Refraction Caused by Induction of Acute Hyperglycemia in Healthy Volunteers</title><title>Japanese journal of ophthalmology</title><addtitle>Jpn J Ophthalmol</addtitle><description>Purpose: To determine whether the myopic changes and ocular hypotension after a glucose load are caused by hyperglycemia.
Methods: Oral glucose tolerance tests were conducted on seven healthy young subjects with normal vision. The changes in the hematologic parameters and the refractive system were measured periodically for 150 minutes after the glucose load.
Results: After the glucose load, there was an increase in plasma glucose level and the level of plasma osmosis, ocular hypotension, a myopic change in refractive power, shallowing of the anterior chamber, and a thickening of the lens. The degree of the myopic change exceeded the power of the residual accommodation. Normalization of the plasma glucose level led to a normalization of the intraocular pressure and a reversal of the myopic changes.
Conclusions: These findings suggest that the myopic changes that accompanied hyperglycemia were caused by a thickening of the lens resulting from a decrease in the tension of the zonule fibers of Zinn, and were secondary to ocular hypotension. Hyperopia appeared to be caused by the reversal of the myopia after normalization of plasma glucose levels.</description><subject>Accommodation, Ocular</subject><subject>Acute Disease</subject><subject>Administration, Oral</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Glucose - administration & dosage</subject><subject>Glucose load</subject><subject>Glucose Tolerance Test</subject><subject>Humans</subject><subject>hyperglycemia</subject><subject>Hyperglycemia - blood</subject><subject>Hyperglycemia - complications</subject><subject>Hyperglycemia - physiopathology</subject><subject>Insulin - blood</subject><subject>Intraocular Pressure</subject><subject>IOP</subject><subject>lens</subject><subject>Lens, Crystalline - physiopathology</subject><subject>Ligaments - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>myopia</subject><subject>Myopia - blood</subject><subject>Myopia - etiology</subject><subject>Myopia - physiopathology</subject><subject>Ocular Hypotension - blood</subject><subject>Ocular Hypotension - etiology</subject><subject>Ocular Hypotension - physiopathology</subject><subject>Somatostatin - administration & dosage</subject><issn>0021-5155</issn><issn>1613-2246</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0M9r2zAUwHFRNpo07Z_Q4sMY7cGrnizL1mmUsDaBwKC_ruJZfm41HDuT7IH_-zl1aHfbSSA-70l8GTsH_g04qOsHzgXEKaTppdZXnHOdx-KIzUFBEgsh1Sc2fyczdhLCrxFJkYhjNgOe5lwpMWfPy1dsXihEronuqfJoO9c20RL7QGVUDNG6Kfvprq2iG9t3FK2GHfmXerC0dbgfXBHW3esQPbd133REPpyyzxXWgc4O54I93f54XK7izc-79fJmE1sJuovJigxUmhegKxRaUabLTECRZ5gKLTMoEEACJpRjnpQyxaxCklJJDoVK8mTBvk57d7793VPozNYFS3WNDbV9MEonkAAXI0wnaH0bgqfK7Lzboh8McLMPat6Cmn0to7V5C2r2cxeHB_piS-U_U1PBEXw5AAwW67FgY134cDqXnKuRfZ8YjTX-OPImWEeNpdJ5sp0pW_efn_wFEHyQzQ</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>Furushima, Masatoshi</creator><creator>Imaizumi, Masamoto</creator><creator>Nakatsuka, Kazuo</creator><general>Elsevier Inc</general><general>Springer</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>19990901</creationdate><title>Changes in Refraction Caused by Induction of Acute Hyperglycemia in Healthy Volunteers</title><author>Furushima, Masatoshi ; Imaizumi, Masamoto ; Nakatsuka, Kazuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-ec271658b19fa296e79d721b87a529471ba1141a3e8a83d45a7fae446401b6383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Accommodation, Ocular</topic><topic>Acute Disease</topic><topic>Administration, Oral</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Glucose - administration & dosage</topic><topic>Glucose load</topic><topic>Glucose Tolerance Test</topic><topic>Humans</topic><topic>hyperglycemia</topic><topic>Hyperglycemia - blood</topic><topic>Hyperglycemia - complications</topic><topic>Hyperglycemia - physiopathology</topic><topic>Insulin - blood</topic><topic>Intraocular Pressure</topic><topic>IOP</topic><topic>lens</topic><topic>Lens, Crystalline - physiopathology</topic><topic>Ligaments - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>myopia</topic><topic>Myopia - blood</topic><topic>Myopia - etiology</topic><topic>Myopia - physiopathology</topic><topic>Ocular Hypotension - blood</topic><topic>Ocular Hypotension - etiology</topic><topic>Ocular Hypotension - physiopathology</topic><topic>Somatostatin - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Furushima, Masatoshi</creatorcontrib><creatorcontrib>Imaizumi, Masamoto</creatorcontrib><creatorcontrib>Nakatsuka, Kazuo</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>Japanese journal of ophthalmology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Furushima, Masatoshi</au><au>Imaizumi, Masamoto</au><au>Nakatsuka, Kazuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in Refraction Caused by Induction of Acute Hyperglycemia in Healthy Volunteers</atitle><jtitle>Japanese journal of ophthalmology</jtitle><addtitle>Jpn J Ophthalmol</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>43</volume><issue>5</issue><spage>398</spage><epage>403</epage><pages>398-403</pages><issn>0021-5155</issn><eissn>1613-2246</eissn><coden>JJOPA7</coden><abstract>Purpose: To determine whether the myopic changes and ocular hypotension after a glucose load are caused by hyperglycemia.
Methods: Oral glucose tolerance tests were conducted on seven healthy young subjects with normal vision. The changes in the hematologic parameters and the refractive system were measured periodically for 150 minutes after the glucose load.
Results: After the glucose load, there was an increase in plasma glucose level and the level of plasma osmosis, ocular hypotension, a myopic change in refractive power, shallowing of the anterior chamber, and a thickening of the lens. The degree of the myopic change exceeded the power of the residual accommodation. Normalization of the plasma glucose level led to a normalization of the intraocular pressure and a reversal of the myopic changes.
Conclusions: These findings suggest that the myopic changes that accompanied hyperglycemia were caused by a thickening of the lens resulting from a decrease in the tension of the zonule fibers of Zinn, and were secondary to ocular hypotension. Hyperopia appeared to be caused by the reversal of the myopia after normalization of plasma glucose levels.</abstract><cop>Heidelberg</cop><pub>Elsevier Inc</pub><pmid>10580662</pmid><doi>10.1016/S0021-5155(99)00098-2</doi><tpages>6</tpages></addata></record> |
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| subjects | Accommodation, Ocular Acute Disease Administration, Oral Adolescent Adult Biological and medical sciences Blood Glucose - metabolism Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Glucose - administration & dosage Glucose load Glucose Tolerance Test Humans hyperglycemia Hyperglycemia - blood Hyperglycemia - complications Hyperglycemia - physiopathology Insulin - blood Intraocular Pressure IOP lens Lens, Crystalline - physiopathology Ligaments - physiopathology Male Medical sciences myopia Myopia - blood Myopia - etiology Myopia - physiopathology Ocular Hypotension - blood Ocular Hypotension - etiology Ocular Hypotension - physiopathology Somatostatin - administration & dosage |
| title | Changes in Refraction Caused by Induction of Acute Hyperglycemia in Healthy Volunteers |
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