Tasha P. Ballard

Sympathetic neural activation in visceral obesity

Background—Muscle sympathetic nerve activity (MSNA) is elevated in obese humans. However, the potential role of abdominal visceral fat as an important adipose tissue depot linking obesity to elevated MSNA has not been explored. Accordingly, we tested the hypothesis that MSNA would be increased in men (age=18 to 40 years, body mass index ≤35 kg/m2) with higher abdominal visceral fat (HAVF; n=13, abdominal visceral fat=118.1±15.8 cm2) compared with their age- (28.7±2.4 versus 25.5±2.0 years, P >0.05), total fat mass-matched (20.6±2.1 versus 20.8±2.4 kg, P >0.05) and abdominal subcutaneous fat-matched (230.6±24.9 versus 261.4±34.8 cm2, P >0.05) peers with lower abdominal visceral fat levels (LAVF; n=13, visceral fat= 73.0±6.0 cm2). Methods and Results—MSNA (microneurography), body composition (dual energy x-ray absorptiometry), and abdominal visceral and subcutaneous fat (computed tomography) were measured in 37 sedentary men across a wide range of adiposity. MSNA was ≈55% higher in men with HAVF compared with men with LAVF (33±4 versus 21±2 bursts/min, P <0.05). Furthermore, MSNA was more closely associated with the level of abdominal visceral fat (r =0.65, P <0.05) than total fat mass (r =0.323, P <0.05) or abdominal subcutaneous fat (r =0.27, P =0.05). The relation between MSNA and abdominal visceral fat was independent of total body fat (r =0.61, P <0.05). Conclusions—The results of our study indicate that MSNA is elevated in men with visceral obesity. Our observations are consistent with the idea that abdominal visceral fat is an important adipose tissue depot linking obesity with sympathetic neural activation in humans. Furthermore, these findings may have important implications for understanding the increased risk of developing cardiovascular diseases in individuals with visceral obesity.

NARINGIN DOES NOT ALTER CAFFEINE PHARMACOKINETICS, ENERGY EXPENDITURE, OR CARDIOVASCULAR HAEMODYNAMICS IN HUMANS FOLLOWING CAFFEINE CONSUMPTION

1 Naringin, a grapefruit constituent interacts with many medications including caffeine, a popular weight loss supplement. The purpose of the current study was to identify changes in caffeine pharmacokinetics, resting energy expenditure (REE), oxygen consumption (VO2) and respiratory exchange ratio (RER) after an acute dosage of caffeine and naringin. 2 Using a double‐blinded, counterbalanced design, REE, VO2, and RER were measured before and systematically for 8 h after a single dosage of caffeine (CAF, 200 mg) with and without naringin (100 mg (CN100) or 200 mg (CN200)) in 10 apparently healthy individuals. A standardized meal was provided following 240‐minute measurements (400 kcals; 35 g carbohydrate; 27 g protein; 7 g fat). 3 Caffeine, CN100, CN200 did not alter VO2 or VO2 area under the curve (137 301 ± 8318, 139 729 ± 9300, 134 297 ± 8318, mL/480 min). Resting energy expenditure (k/cals) was 10.0 ± 1.4% higher with CAF versus CN200 (6.0 ± 1.4%) and CN100 (6 ± 1.5%) at 240 min (P = 0.07) which was then negated following a standardized meal. Percent change in RER from pre to 240 min and pre to 480 min was not different between the CAF, CN100, or CN200 (–0.2 ± 1.7%, 1.7 ± 1.7%, –2.8 ± 1.9%). 4 Although caffeine alone suggests a trend of increased REE, the results of the present study indicate that concurrent consumption of caffeine with naringin in acute dosages does not affect RER, VO2, and prevents the increase of REE in adult humans. The results suggest that the interaction of grapefruit juice and caffeine may be due to constituents of grapefruit juice other than naringin or in addition to naringin.