PMID- 22108527 OWN - NLM STAT- MEDLINE DCOM- 20120403 LR - 20211021 IS - 1475-2840 (Electronic) IS - 1475-2840 (Linking) VI - 10 DP - 2011 Nov 22 TI - Dysglycemia induces abnormal circadian blood pressure variability. PG - 104 LID - 10.1186/1475-2840-10-104 [doi] AB - BACKGROUND: Prediabetes (PreDM) in asymptomatic adults is associated with abnormal circadian blood pressure variability (abnormal CBPV). HYPOTHESIS: Systemic inflammation and glycemia influence circadian blood pressure variability. METHODS: Dahl salt-sensitive (S) rats (n = 19) after weaning were fed either an American (AD) or a standard (SD) diet. The AD (high-glycemic-index, high-fat) simulated customary human diet, provided daily overabundant calories which over time lead to body weight gain. The SD (low-glycemic-index, low-fat) mirrored desirable balanced human diet for maintaining body weight. Body weight and serum concentrations for fasting glucose (FG), adipokines (leptin and adiponectin), and proinflammatory cytokines [monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha)] were measured. Rats were surgically implanted with C40 transmitters and blood pressure (BP-both systolic; SBP and diastolic; DBP) and heart rate (HR) were recorded by telemetry every 5 minutes during both sleep (day) and active (night) periods. Pulse pressure (PP) was calculated (PP = SBP-DBP). RESULTS: [mean(SEM)]: The AD fed group displayed significant increase in body weight (after 90 days; p < 0.01). Fasting glucose, adipokine (leptin and adiponectin) concentrations significantly increased (at 90 and 172 days; all p < 0.05), along with a trend for increased concentrations of systemic pro-inflammatory cytokines (MCP-1 and TNF-alpha) on day 90. The AD fed group, with significantly higher FG, also exhibited significantly elevated circadian (24-hour) overall mean SBP, DBP, PP and HR (all p < 0.05). CONCLUSION: These data validate our stated hypothesis that systemic inflammation and glycemia influence circadian blood pressure variability. This study, for the first time, demonstrates a cause and effect relationship between caloric excess, enhanced systemic inflammation, dysglycemia, loss of blood pressure control and abnormal CBPV. Our results provide the fundamental basis for examining the relationship between dysglycemia and perturbation of the underlying mechanisms (adipose tissue dysfunction induced local and systemic inflammation, insulin resistance and alteration of adipose tissue precursors for the renin-aldosterone-angiotensin system) which generate abnormal CBPV. FAU - Kumarasamy, Sivarajan AU - Kumarasamy S AD - Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA. FAU - Gopalakrishnan, Kathirvel AU - Gopalakrishnan K FAU - Kim, Dong Hyun AU - Kim DH FAU - Abraham, Nader G AU - Abraham NG FAU - Johnson, William D AU - Johnson WD FAU - Joe, Bina AU - Joe B FAU - Gupta, Alok K AU - Gupta AK LA - eng GR - P01 HL034300/HL/NHLBI NIH HHS/United States GR - R01 HL076709/HL/NHLBI NIH HHS/United States GR - R01 HL020176/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Extramural DEP - 20111122 PL - England TA - Cardiovasc Diabetol JT - Cardiovascular diabetology JID - 101147637 RN - 0 (Adiponectin) RN - 0 (Adipoq protein, rat) RN - 0 (Biomarkers) RN - 0 (Blood Glucose) RN - 0 (Ccl2 protein, rat) RN - 0 (Chemokine CCL2) RN - 0 (Inflammation Mediators) RN - 0 (Leptin) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Adiponectin/blood MH - Animals MH - Biomarkers/blood MH - Blood Glucose/*metabolism MH - *Blood Pressure MH - Blood Pressure Monitoring, Ambulatory MH - Chemokine CCL2/blood MH - *Circadian Rhythm MH - Diet, High-Fat MH - Disease Models, Animal MH - Heart Rate MH - Inflammation/blood/etiology/*physiopathology MH - Inflammation Mediators/blood MH - Leptin/blood MH - Prediabetic State/blood/etiology/*physiopathology MH - Rats MH - Rats, Inbred Dahl MH - Telemetry MH - Time Factors MH - Tumor Necrosis Factor-alpha/blood MH - Weight Gain PMC - PMC3247849 EDAT- 2011/11/24 06:00 MHDA- 2012/04/04 06:00 PMCR- 2011/11/22 CRDT- 2011/11/24 06:00 PHST- 2011/09/12 00:00 [received] PHST- 2011/11/22 00:00 [accepted] PHST- 2011/11/24 06:00 [entrez] PHST- 2011/11/24 06:00 [pubmed] PHST- 2012/04/04 06:00 [medline] PHST- 2011/11/22 00:00 [pmc-release] AID - 1475-2840-10-104 [pii] AID - 10.1186/1475-2840-10-104 [doi] PST - epublish SO - Cardiovasc Diabetol. 2011 Nov 22;10:104. doi: 10.1186/1475-2840-10-104.