Abstract
BackgroundPrediabetes (PreDM) in asymptomatic adults is associated with abnormal circadian blood pressure variability (abnormal CBPV).HypothesisSystemic inflammation and glycemia influence circadian blood pressure variability.MethodsDahl 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-α (TNF-α)] 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-α) 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).ConclusionThese 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.
Highlights
Prediabetes (PreDM) in asymptomatic adults is associated with abnormal circadian blood pressure variability.Hypothesis: Systemic inflammation and glycemia influence circadian blood pressure variability
Our results provide the fundamental basis for examining the relationship between dysglycemia and perturbation of the underlying mechanisms which generate abnormal CBPV
There were no significant differences in the mean body weight of the group fed with the American diet (AD) in comparison with the group fed standard diet (SD) at 90 days
Summary
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. The secreted adipokines (including cytokines and chemokines) mediating auto, para and endocrine actions, alter the dynamic homeostatic milieu to enhance systemic inflammation, which results in dysglycemia, dyslipidemia, and/or a loss of control of blood pressure [3,4,5,6]. These early changes are clinically manifest as prediabetes and prehypertension, in advance of the chronic changes that subsequently (at times years later) lead to a diagnosis of diabetes mellitus and hypertension [4,7]. Prediabetes and prehypertension in otherwise healthy adults singly, or together (co-existing prediabetes and prehypertension) place the individual on a pathway with potential for accelerated cardiovascular adverse events, including sudden death [10,11,12,13]
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