Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/20853
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dc.contributor.authorBaqar, Sara-
dc.contributor.authorStraznicky, Nora E-
dc.contributor.authorLambert, Gavin-
dc.contributor.authorKong, Yee Wen-
dc.contributor.authorDixon, John B-
dc.contributor.authorJerums, George-
dc.contributor.authorEkinci, Elif Ilhan-
dc.contributor.authorLambert, Elisabeth-
dc.date2019-
dc.date.accessioned2019-06-05T01:28:39Z-
dc.date.available2019-06-05T01:28:39Z-
dc.date.issued2019-
dc.identifier.citationBMJ Open Diabetes Research & Care 2019; 7(1): e000606-
dc.identifier.issn2052-4897-
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/20853-
dc.description.abstractLow sodium intake may trigger sympathetic nervous system (SNS) activation and endothelial dysfunction. Studies have not explored these associations along the glucose continuum. Accordingly, we compared endothelial function and SNS activity in individuals with low sodium intake and differing categories of metabolic risk along the glucose continuum. We hypothesized that low sodium intake is associated with (1) impairment of endothelial function and (2) higher SNS activity in individuals with higher metabolic risk. In this prospective observational study, participants (n=54) with low sodium intake (single 24 hours urine sodium excretion <150 mmol/24 hours) were categorized based on oral glucose tolerance testing as: normal glucose tolerance (NGT, n=10), impaired glucose tolerance (IGT, n=15), treatment naive type 2 diabetes (T2D-) (n=12) or treated type 2 diabetes (T2D+) (n=17). We assessed endothelial function using pulse amplitude tonometry (PAT) derived reactive hyperemic index and PAT ratio; arterial stiffness via augmentation index; muscle sympathetic nerve activity (MSNA) using microneurography; cardiac baroreflex; heart rate; blood pressure; glycosylated hemoglobin A1c (HbA1c) and lipid profile. Mean (SD) sodium excretion was 110.6 (26) mmol/24 hours. Compared with NGT, IGT and T2D-, the T2D+ group had lower MSNA (p=0.005), PAT ratio (p=0.04) and baroreflex sensitivity (p=0.0002) and an augmented heart rate (p=0.02). The T2D+ group had appropriate mean (SD) glycemic (HbA1c 7.2 (1.72)%), total cholesterol (4.2 (1.0) mmol/L), low-density lipoprotein (2.2 (1.0) mmol/L) and blood pressure (systolic 136 (13), diastolic 78 (12)) (mm Hg) control. Individuals with T2D+ have impaired endothelial and baroreflex function, despite low sodium intake, appropriately managed cardiometabolic risk factors and lower SNS activity, compared with others along the glucose continuum. Whether low sodium intake is associated with modulation of the sympathovascular profile in T2D requires further investigation.-
dc.language.isoeng-
dc.subjectcardiovascular disease-
dc.subjectendothelial dysfunction-
dc.subjectimpaired glucose tolerance-
dc.subjectmicroneurography-
dc.subjectpulse amplitude tonometry-
dc.subjectsympathetic nervous system-
dc.subjecttwenty four hour urinary sodium excretion-
dc.subjecttype 2 diabetes-
dc.titleComparison of endothelial function and sympathetic nervous system activity along the glucose continuum in individuals with differing metabolic risk profiles and low dietary sodium intake.-
dc.typeJournal Article-
dc.identifier.journaltitleBMJ Open Diabetes Research & Care-
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Human Neurotransmitters Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australiaen
dc.identifier.affiliationFaculty of Health, Arts and Design, Iverson Health Innovation Research Institute, Swinburne University of Technology, Melbourne, Victoria, Australiaen
dc.identifier.affiliationVascular and Hypertension, Obesity Research, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australiaen
dc.identifier.affiliationFaculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Endocrinology, Austin Health, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1136/bmjdrc-2018-000606-
dc.identifier.orcid0000-0002-4921-1349-
dc.identifier.orcid0000-0003-2372-395X-
dc.identifier.orcid0000-0002-2232-9048-
dc.identifier.pubmedid31114697-
dc.type.austinJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.languageiso639-1en-
item.fulltextNo Fulltext-
crisitem.author.deptEndocrinology-
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