title: Increased circulating ANG II and TNF-α represents important risk factors in obese saudi adults with hypertension irrespective of diabetic status and BMI.
abstract: Central adiposity is a significant determinant of obesity-related hypertension risk, which may arise due to the pathogenic inflammatory nature of the abdominal fat depot. However, the influence of pro-inflammatory adipokines on blood pressure in the obese hypertensive phenotype has not been well established in Saudi subjects. As such, our study investigated whether inflammatory factors may represent useful biomarkers to delineate hypertension risk in a Saudi cohort with and without hypertension and/or diabetes mellitus type 2 (DMT2). Subjects were subdivided into four groups: healthy lean controls (age: 47.9±5.1 yr; BMI: 22.9±2.1 Kg/m(2)), non-hypertensive obese (age: 46.1±5.0 yr; BMI: 33.7±4.2 Kg/m(2)), hypertensive obese (age: 48.6±6.1 yr; BMI: 36.5±7.7 Kg/m(2)) and hypertensive obese with DMT2 (age: 50.8±6.0 yr; BMI: 35.3±6.7 Kg/m(2)). Anthropometric data were collected from all subjects and fasting blood samples were utilized for biochemical analysis. Serum angiotensin II (ANG II) levels were elevated in hypertensive obese (p<0.05) and hypertensive obese with DMT2 (p<0.001) compared with normotensive controls. Systolic blood pressure was positively associated with BMI (p<0.001), glucose (p<0.001), insulin (p<0.05), HOMA-IR (p<0.001), leptin (p<0.01), TNF-α (p<0.001) and ANG II (p<0.05). Associations between ANG II and TNF-α with systolic blood pressure remained significant after controlling for BMI. Additionally CRP (p<0.05), leptin (p<0.001) and leptin/adiponectin ratio (p<0.001) were also significantly associated with the hypertension phenotype. In conclusion our data suggests that circulating pro-inflammatory adipokines, particularly ANG II and, TNF-α, represent important factors associated with a hypertension phenotype and may directly contribute to predicting and exacerbating hypertension risk.
authors.affiliation: Biomarkers Research Program, Department of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia. aldaghri2011@gmail.com
authors.forename: Nasser M
authors.initials: NM
authors.lastname: Al-Daghri
authors.forename: Lotfi S
authors.initials: LS
authors.lastname: Bindahman
authors.forename: Omar S
authors.initials: OS
authors.lastname: Al-Attas
authors.forename: Tahia H
authors.initials: TH
authors.lastname: Saleem
authors.forename: Majed S
authors.initials: MS
authors.lastname: Alokail
authors.forename: Khalid M
authors.initials: KM
authors.lastname: Alkharfy
authors.forename: Hossam M
authors.initials: HM
authors.lastname: Draz
authors.forename: Sobhy
authors.initials: S
authors.lastname: Yakout
authors.forename: Amany O
authors.initials: AO
authors.lastname: Mohamed
authors.forename: Alison L
authors.initials: AL
authors.lastname: Harte
authors.forename: Philip G
authors.initials: PG
authors.lastname: McTernan
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000097:blood*; D001794:Blood Pressure; D015992:Body Mass Index; D048909:Diabetes Complications; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000150:complications; D012307:Risk Factors; D012529:Saudi Arabia; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D000804:Angiotensin II