High-Fat Food, Sympathetic Nerve Activity, and Hypertension

Abstract

See related article, pp 1498–1502 Obesity is a rapidly escalating epidemic accounting for more than $150 billion per year in healthcare expenditures in the United States, more than any other medical condition. The consequences are severe. Obese humans exhibit increased incidence of type II diabetes mellitus, obstructive sleep apnea, hypertension, and regionally specific sympathoexcitation, in particular to the kidneys and legs.1–4 However, whether increased sympathetic nerve activity (SNA) is a cause or a consequence of obesity has been debated.3 Moreover, although obesity-induced hypertension is associated with increased SNA, the mechanisms are unclear.1–4 Two recent articles5,6 in Hypertension address these questions by characterizing the time course of the increases in SNA, monitored using telemetry, as lean animals initiate a high-fat diet (HFD). In the article by Armitage et al,5 male New Zealand white rabbits were instrumented for telemetric recordings of arterial pressure (AP) and renal SNA (RSNA). One week later, blood samples were collected for the measurements of glucose, insulin, and leptin, and basal levels of AP, heart rate (HR), and RSNA were measured in the laboratory. Rabbits were then randomized into 2 groups: 1 group was fed 110 g/d of standard rabbit chow (4.2% fat) and the other 190 g/d of a HFD (standard diet with 13.3% fat). Weekly measurements continued for 3 weeks and after a 1-week recovery period. After 1 week, HFD-fed rabbits exhibited elevations in AP (by 6%), HR (by 11%), and RSNA (by ≈50%), in association with increments in body weight, fat mass, and plasma glucose, insulin, and leptin levels. The increases in HR, RSNA, glucose, insulin, and leptin remained level for the subsequent 2 weeks, whereas body weight and AP increased further. Interestingly, during the recovery period, glucose, insulin, leptin, and HR returned to …