Introduction: Obesity is strongly linked to hypertension and cardiovascular disease (CVD), especially when present from early life, but the underlying mechanisms are unclear. Blunted sympathetic inhibition of gut blood flow after meals has been observed in overweight animals and suggested as a promotor of hypertensive CVD. This possibility had not been examined in humans so we tested it by measuring cardiovascular and adrenomedullar responses to food ingestion in normal weight and overweight/obese (OW/OB) teenagers.
Methods: Eighty-two healthy adolescents (40 OW/OB) were enrolled. Rapid MRI was used to measure global and regional hemodynamic responses to ingestion of a high-calorie liquid meal, as well as LV mass. Serial blood samples were collected to determine epinephrine levels and an index of fasting insulin resistance.
Results: OW\OB was associated with lower total peripheral resistance, higher circulating volume and higher systolic BP. Food ingestion increased cardiac output, heart rate, BP and blood flow to the gut and kidneys but decreased blood flow to the upper limbs and head. Circulating epinephrine decreased. Greater BMI z-score was associated with blunting of the blood flow response in the gut and a smaller decrease or paradoxical increase of epinephrine levels. Blunted mesenteric blood flow responses were associated with increased LV mass index, independently of insulin resistance and fasting BP. Moreover, OW/OB subjects with an abnormal epinephrine response had a hypertensive BP response to the meal.
Conclusions: We present the first human evidence that disordered postprandial gut blood flow regulation is linked to OW\OB in adolescence; is likely to be due to abnormal sympathetic nervous system function and is associated with higher BP and greater LV mass. Given that most people in the developed world are in a post-prandial state for as much as 12 hours per day, these findings suggest a potential pathway to CVD that deserves further attention.