Modest weight gain is associated with sympathetic neural activation in nonobese humans

2007 ◽  
Vol 292 (5) ◽  
pp. R1834-R1838 ◽  
Author(s):  
Christopher L. Gentile ◽  
Jeb S. Orr ◽  
Brenda M. Davy ◽  
Kevin P. Davy

We tested the hypothesis that modest, overfeeding-induced weight gain would increase sympathetic neural activity in nonobese humans. Twelve healthy males (23 ± 2 years; body mass index, 23.8 ± 0.7) were overfed ∼1,000 kcal/day until a 5-kg weight gain was achieved. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, body composition (dual energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 wk of weight stability at each individual's elevated body weight. Overfeeding increased body weight (73.5 ± 3.1 vs. 78.4 ± 3.2 kg, P < 0.001) and body fat (14.9 ± 1.2 vs. 18 ± 1.1 kg, P < 0.001) in 42 ± 8 days. Total abdominal fat increased (220 ± 22 vs. 266 ± 22 cm2, P < 0.001) with weight gain, due to increases in both subcutaneous (158 ± 15 vs. 187 ± 12 cm2, P < 0.001) and visceral fat (63 ± 8 vs. 79 ± 12 cm2, P = 0.004). As hypothesized, weight gain elicited increases in MSNA burst frequency (32 ± 2 vs. 38 ± 2 burst/min, P = 0.002) and burst incidence (52 ± 4 vs. 59 ± 3 bursts/100 heart beats, P = 0.026). Systolic, but not diastolic blood pressure increased significantly with weight gain. The change in MSNA burst frequency was correlated with the percent increase in body weight ( r = 0.59, P = 0.022), change in body fat ( r = 0.52, P = 0.043) and percent change in body fat ( r = 0.51, P = 0.045). The results of the current study indicate that modest diet-induced weight gain elicits sympathetic neural activation in nonobese males. These findings may have important implications for understanding the link between obesity and hypertension.

2011 ◽  
Vol 212 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Michael Mangubat ◽  
Kabirullah Lutfy ◽  
Martin L Lee ◽  
Laura Pulido ◽  
David Stout ◽  
...  

Nicotine induces weight loss in both humans and rodents consuming a regular diet; however, the effect of nicotine on body weight and fat composition in rodents consuming a high-fat diet (HFD) has not been well studied. Thus, this study examined the effect of nicotine vs saline on body weight and fat composition in mice fed with either an HFD (62% of kcal from fat) or a standard normal chow diet (NCD) for 7 weeks. Nicotine dose dependently reduced body weight gain in mice that consumed both diets, but this effect was significantly greater in mice on the HFD. Caloric intake was decreased in nicotine-treated mice. Estimates of energy intake suggested that decreased caloric intake accounted for all the reduced weight gain in mice on an NCD and 66% of the reduced weight gain on an HFD. Computed tomography analysis for fat distribution demonstrated that nicotine was effective in reducing abdominal fat in mice that consumed the HFD, with nicotine treatment leading to lower visceral fat. The effect of nicotine on weight loss in mice on an HFD was completely blocked by mecamylamine, a nonselective nicotinic acetylcholine receptor (nAChR) antagonist, but only partially blocked by the α4β2 nAChR partial agonist/antagonist, varenicline. We conclude that nicotine is effective in preventing HFD-induced weight gain and abdominal fat accumulation.


Author(s):  
Magnus Dencker ◽  
Anton Danielson ◽  
Magnus K. Karlsson ◽  
Per Wollmer ◽  
Lars B. Andersen ◽  
...  

AbstractBackground:The aim of the study was to assess possible relationships between adipocyte fatty acid-binding protein (FABP4) and total body fat (TBF), abdominal fat, body fat distribution, aerobic fitness, blood pressure, cardiac dimensions and the increase in body fat over 2 years in a community sample of children.Methods:A cross-sectional study was used in a community sample of 170 (92 boys and 78 girls) children aged 8–11 years. TBF and abdominal fat (AFM) were measured by dual-energy X-ray absorptiometry (DXA). TBF was also expressed as percentage of total body mass (BF%), and body fat distribution was calculated as AFM/TBF. Maximal oxygen uptake (VOResults:Partial correlations, with adjustment for sex, between FABP4 vs. ln TBF, ln BF%, ln AFM, AFM/TBF and VOConclusions:Findings from this community-based cohort of young children show that increased body fat and abdominal fat, more abdominal body fat distribution, low fitness, more LVM and increased LA, increased SBP and PP were all associated with increased levels of FABP4. Increase in TBF and abdominal fat over 2 years were also associated with increased levels of FABP4.


1995 ◽  
Vol 80 (4) ◽  
pp. 1118-1123 ◽  
Author(s):  
H S Glauber ◽  
W M Vollmer ◽  
M C Nevitt ◽  
K E Ensrud ◽  
E S Orwoll

1993 ◽  
Vol 75 (2) ◽  
pp. 663-667 ◽  
Author(s):  
M. Saito ◽  
A. Tsukanaka ◽  
D. Yanagihara ◽  
T. Mano

The aim of this study was to clarify the relationship between sympathetic outflow to skeletal muscle and oxygen uptake during dynamic exercise. Muscle sympathetic nerve activity (MSNA) was recorded from the right median nerve microneurographically in eight healthy volunteers during leg cycling at four different intensities in a seated position for a 16-min bout. Work loads selected were 20, 40, 60, and 75% of maximal oxygen uptake (VO2max). Heart rate and blood pressure were measured during each exercise test. MSNA burst frequency was suppressed by 28% during cycling at 20% VO2max (23 vs. 33 bursts/min for control). Thereafter, it increased in a linear fashion with increasing work rate, with a significantly higher burst frequency during 60% VO2max than the control value. Both heart rate and mean blood pressure rose significantly during 20% VO2max from the control value and increased linearly with increased exercise intensity. During light exercise, MSNA was suppressed by arterial and cardiopulmonary baroreceptors as a result of the hemodynamic changes associated with leg muscle pumping. The baroreflex inhibition may overcome the muscle metaboreflex excitation to induce MSNA suppression during light exercise. These results suggest that during light exercise MSNA is inhibited, perhaps due to loading of the cardiopulmonary and arterial baroreflexes, and that during heavier exercise the increase in MSNA occurs as muscle metaboreflexes are activated.


2011 ◽  
Vol 6 (2-2) ◽  
pp. e597-e602 ◽  
Author(s):  
Magnus Dencker ◽  
Per Wollmer ◽  
Magnus K. Karlsson ◽  
Christian Lindén ◽  
Lars B. Andersen ◽  
...  

2019 ◽  
Vol 105 (4) ◽  
pp. e1187-e1200 ◽  
Author(s):  
Sara Baqar ◽  
Yee Wen Kong ◽  
Angela X Chen ◽  
Christopher O’Callaghan ◽  
Richard J MacIsaac ◽  
...  

Abstract Context Lower sodium intake is paradoxically associated with higher mortality in type 2 diabetes (T2D). Objective To determine whether sympathetic nervous system (SNS) activation and endothelial dysfunction contribute to these observations, we examined the effect of salt supplementation on these systems in people with T2D with habitual low sodium. We hypothesized that salt supplementation would lower SNS activity and improve endothelial function compared to placebo. Design We conducted a randomized, double-blinded, placebo-controlled crossover trial. Setting The study took place in a tertiary referral diabetes outpatient clinic. Participants Twenty-two people with T2D with habitual low sodium intake (24-hour urine sodium &lt;150 mmol/24h) were included. Intervention Salt supplementation (100 mmol NaCl/24h) or placebo for 3 weeks was administered. Main outcome measures The primary outcome of SNS activity and endothelial function was assessed as follows: Microneurography assessed muscle sympathetic nerve activity (MSNA), pulse amplitude tonometry assessed endothelial function via reactive hyperemic index (RHI), and arterial stiffness was assessed via augmentation index (AI). Secondary outcomes included cardiac baroreflex, serum aldosterone, ambulatory blood pressure monitoring (ABPM), heart rate variability (HRV), and salt sensitivity. Results Compared to placebo, salt supplementation increased MSNA (burst frequency P = .047, burst incidence P = .016); however, RHI (P = .24), AI (P = .201), ABPM (systolic P = .09, diastolic P = .14), and HRV were unaffected. Salt supplementation improved baroreflex (slope P = .026) and lowered aldosterone (P = .004), and in salt-resistant individuals there was a trend toward improved RHI (P = .07). Conclusions In people with T2D and low habitual sodium intake, salt supplementation increased SNS activity without altering endothelial function or blood pressure but improved baroreflex function, a predictor of cardiac mortality. Salt-resistant individuals trended toward improved endothelial function with salt supplementation.


2021 ◽  
Vol 42 (6supl2) ◽  
pp. 4009-4022
Author(s):  
Thiago Rodrigues da Silva ◽  
◽  
Karina Márcia Ribeiro de Souza Nascimento ◽  
Charles Kiefer ◽  
Luanna Lopes Paiva Copat ◽  
...  

The present study proposes to examine the effect of dietary levels of metabolizable energy, under a fixed nutrient:calorie ratio, on the production performance; body fat and protein deposition; and carcass characteristics of free-range broilers from 1 to 84 days of age. Nine hundred unsexed chicks were allocated to six treatments in a completely randomized design with six replicates of 25 birds each. Treatments consisted of diets with varying levels of metabolizable energy (2700, 2800, 2900, 3000, 3100 and 3200 Kcal ME/kg of diet) and a fixed proportion of nutrients relative to the energy level according to the nutritional requirements for each rearing phase. Body weight, weight gain, feed intake, feed conversion, production viability, metabolizable energy intake, protein intake, lysine intake, body fat deposition, body protein deposition and carcass characteristics were evaluated. Data were subjected to analysis of variance and, later, to regression analysis. Increasing levels of metabolizable energy, coupled with a fixed nutrient:calorie ratio, reduced feed intake, increased body weight and weight gain, improved feed conversion and did not affect carcass characteristics. In conclusion, adjusting the nutrient supply according to the dietary energy level improves production performance by improving feed conversion, ensuring adequate nutrient intake and preserving fat and protein deposition in the carcass when the metabolizable energy level is raised up to 3200 Kcal/kg in all rearing stages.


2021 ◽  
Vol 19 (1) ◽  
pp. 21-28
Author(s):  
P. Tayfur ◽  
K. Gökçe Tezel ◽  
Ö. Barutçu ◽  
S. Yılmaz ◽  
E. Ö. Özgür ◽  
...  

A fructose-rich diet has been known to cause metabolic syndrome effects such as body weight gain, increased blood pressure, blood lipids and glucose levels. The role of voluntary physical activity in these alterations is not known clearly. The aim of this study was to investigate the possible improving effects of voluntary physical activity in rats that were feeding with a fructose-rich diet. Spraque-Dawley female rats were separated as control (C;n=7), voluntary physical activity (A;n=7), fructose (F;n=7) and fructose+activity (F+A;n=7) groups. A and FA groups were kept in cages with running wheels during six weeks. F and FA groups were fed with adding 20% fructose in drinking water. Body weight was measured weekly and Lee Index was used to determine obesity. At the end of the feeding period serum glucose, insulin and lipid levels were measured by enzymatic method and blood pressure was determined with the tail-cuff method. Daily voluntary walking distance in F+A and A groups were similar during six weeks. Fructose intake induced to increase systolic blood pressure (p=0.001), diastolic blood pressure (p=0.002), glucose (p=0.041), insulin (p=0.001), cholesterol (p=0.001), triglyceride (p=0.001) and liver weight (p=0.035). The voluntary activity was found effective on the decrease of weight gain (p=0.018) however we did not observe a significant effect on blood pressure (p=0.917) and insulin resistance (p=0.565) following the fructose-rich diet. We conclude that voluntary activity has preventive effect on obesity but may not to be effective on increased blood pressure and insulin resistance in female rats which were feeding fructose-rich diet during six weeks.


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