Relationship between changes in serum leptin levels and blood pressure after weight loss.

Insulin resistance is thought to raise blood pressure. Recently, a significant positive relationship between mean blood pressure and plasma leptin levels, but there have been no reports dealing with the relationship between blood pressure and either insulin resistance or serum leptin levels after weight loss. In the present work, we attempted to clarify the relationship between changes in blood pressure and either the serum leptin level or the insulin level in 102 moderately obese females (mean body mass index (BMI), 29.5 +/- 0.5 kg/m2; age, 47.0 +/- 0.9) during a 3 month period. No differences in age, fat-mass, homeostasis model assessment (HOMA), the summation of insulin (sigmaIRI), plasma renin activity (PRA) or 24 h norepinephrine excretion (24hU-NE) were observed between the hypertensive (HT) group (n = 31) and normotensive (NT) group (n = 71) before weight loss, but the basal serum leptin was significantly higher in the HT (16.8 +/- 1.1 ng/ml) than in the NT group (15.2 +/- 0.8 ng/ml), after adjusting for abdominal total fat. After a 3 month weight reduction program, the total abdominal fat, serum leptin and sigmaIRI significantly decreased in both groups. The systolic blood pressure (SBP)/diastolic blood pressure (DBP) significantly decreased from 144/84 to 130/77 mmHg only in the HT but not in the NT group. The PRA decreased in both groups, while the 24hU-NE significantly decreased only in the HT group. The changes in the leptin level were significantly correlated with the changes in both sigmaIRI and HOMA after weight loss in the two groups, respectively. Finally, a statistically significant positive correlation was observed between the changes in the leptin and the changes in the mean blood pressure (MBP) (r = 0.412, p < 0.05) only in the HT group. Multiple regression analysis revealed that the changes in MBP were independently associated with the changes in 24hU-NE and the changes in either sigmaIRI or HOMA in all subjects. However, a statistically significant positive correlation was observed between the changes in MBP and the changes in leptin levels even after adjusting for the total abdominal fat, 24hU-NE and either sigmaIRI or HOMA (both expressed as a percentage of the baseline value) in a multiple regression analysis only in the HT group. These results suggest that leptin may play a role in the pathophysiology of obese hypertension.     

Relationships of the systolic blood pressure response during exercise with insulin resistance,obesity, and endurance fitness in men with type 2 diabetes mellitus

The purpose of the present study was to investigate the relationships among the resting systolic (SBP) and diastolic blood pressure (DBP) or SBP response during exercise with insulin resistance evaluated by a homeostasis model (HOMA-IR), abdominal fat accumulation (visceral fat area [VFA], subcutaneous fat area [SFA]) by computed tomography (CT), and an estimation of the maximal oxygen uptake (V*O2max) in 63 Japanese middle-aged male patients with type 2 diabetes mellitus (type 2 DM). Body mass index (BMI) and waist-to-hip ratio (WHR) in type 2 DM subjects were significantly higher than in age-matched healthy male control subjects (n = 135) with normal glucose tolerance. Resting SBP (127.7 +/- 16.2 mm Hg v 119.4 +/- 13.0 mm Hg) and DBP (82.2 +/- 11.9mmHg v 76.8 +/- 9.4 mm Hg) levels, and the percentage of hypertension (20.6% v 1.5%) in type 2 DM subjects were significantly higher than in the control subjects (P <.05). According to a multiple regression analysis for resting blood pressure in type 2 DM, VFA was found to be an independent predictor of SBP, while V*O2max and HOMA-IR were independent predictors of DBP. In the controls, however, HOMA-IR was not found to be a significantly independent predictor for either resting SBP or resting DBP. Measurement of the SBP response during graded exercise using a ramp test was performed by an electrical braked cycle ergometer in 54 patients with type 2 DM only. The SBP was measured at 15-second intervals during exercise. The exercise intensity at the double product breaking point (DPBP), which strongly correlated with the exercise intensity at the lactate threshold, was used as an index for the SBP response to standardized exercise intensity. The SBP corresponding to exercise intensity at DPBP (SBP@DPBP) was evaluated as an index of the SBP response to standardized exercise intensity. The change in SBP (deltaSBP = SBP@DPBP - resting SBP) was significantly and positively associated with log area under the curve for glucose (log AUCPG) during a 75-g oral glucose tolerance test (OGTT). In addition, deltaSBP significantly and negatively correlated with the log area under the curve for insulin (log AUCIRI) and log AUCIRI/log AUCPG. Based on these results, insulin resistance was suggested to be independently associated with the resting DBP and SBP response to standardized exercise intensity in type 2 DM patients.     

Elevated blood pressure in obese children: influence of gender, age, weight and serum insulin levels

Prepubescent and early pubescent obese children (n = 114, mean percent IBW = 165, mean age 7.3 years) were studied to determine the relationship of weight (WT), percent of ideal body weight (percent IBW), gender, and insulin (I) to systolic (SBP) and diastolic (DBP) blood pressure. Subjects were assessed for weight, height, percent IBW, systolic and diastolic blood pressure, and Tanner stage; subjects with Tanner stage greater than 3 were excluded. Multiple regression revealed that body weight accounted for the greatest variance in SBP (adj. R2 = 0.34, P less than 0.05), followed by the age. For DBP, weight also accounted for the greatest variance (adj. R2 = 0.16, P less than 0.05) followed by gender. A subgroup (n = 50) was evaluated for oral glucose tolerance. Subjects ingested 1.75 g glucose (GLU)/kg weight and had blood samples drawn at 0, 30, 60, 90, 120 and 180 min. Pearson correlations showed SBP correlated significantly to I at 0 (r = 0.44) and the total integrated area for insulin (r = 0.45); however, adjusting SBP for age by using z-score transformations negated all correlations between SBP and insulin. GLU at 0 and the total integrated area were not significantly correlated to SBP or DBP in absolute or age-adjusted terms. These data on prepubescent, nondiabetic, obese children suggest an association between insulin and elevations in SBP, but not DBP, that is largely due to a mutual association between age and weight. Also, insulin resistance as reflected in GLU response was not related to SBP or DBP.     

Decrease in visceral fat following diet-induced weight loss in upper body compared to lower body obese premenopausal women

BACKGROUND: Obesity is associated with numerous metabolic disturbances, such as insulin resistance, diabetes mellitus type 2, dyslipidemia, and hypertension. An excess of fat within the abdomen, so-called visceral adiposity, confers a greater and independent health risk of metabolic and cardiovascular complications than does adipose tissue accumulation elsewhere. The present study aimed to investigate a possible differential effect of diet-induced weight loss in visceral fat mass and metabolic parameters in obese individuals with the upper body (UBO) and lower body (LBO) obese phenotype. METHODS: The obese subjects were prescribed a liquid, very-low calorie diet to reduce 50% of their overweight (15% body weight loss). Specific body fat measurements (MRI, BIA), anthropometrics, and fasting metabolic parameters were obtained in control subjects and two groups of obese subjects (UBO and LBO) before and after weight loss. RESULTS: Weight loss was accompanied by significant decreases in total, subcutaneous, and visceral fat in both UBO and LBO women. The largest reduction in visceral fat mass was found in the UBO women (absolute decrease 223+/-32 cm(2) vs 122+/-91 cm(2) in LBO women; P=0.01), while the amount of visceral fat was reduced to normal levels in LBO women (155+/-25 cm(2) after weight loss vs 143+/-17 cm(2) in controls; P=NS). Furthermore, weight loss significantly lowered fasting glucose, total cholesterol, and LDL cholesterol concentrations in UBO women. CONCLUSION: The obese phenotype is preserved after body weight loss. UBO women have to lose a larger amount of overweight in order to bring the amount of fat in the visceral depot down to normal levels and to obtain normalization of their cardiovascular risk profile.     

Effect of weight loss and regional fat distribution on plasma leptin concentration in obese women.

OBJECTIVES: To investigate how circulating leptin concentrations are related to regional fat distribution and whether moderate weight loss alters these relationships. DESIGN: A 6 month, clinical weight reduction trial with measurements before and after weight loss. SUBJECTS: 38 healthy, obese women (age: 44.3+/-9.9 y, BMI: 34.0+/-4.0 kg/m2). MEASUREMENTS: The following measurements were made. 1. indices of obesity and fat distribution: weight, body mass index (BMI), hip circumference (peripheral fat), waist circumference, total body fat (bioelectrical impedance), abdominal fat distribution: visceral fat and abdominal subcutaneous fat (ultrasonography); and 2. Biochemical measurements: plasma leptin and serum insulin. RESULTS: Baseline plasma leptin concentrations were three-fold higher in obese women than in normal weight controls. After weight loss averaging 8.4 kg (9.0%), plasma leptin decreased by a mean of 22.3% (P < 0.001), corresponding to body fat decrease of 16.6% (P < 0.001), abdominal subcutaneous fat decrease of 17.4% (P < 0.001) and visceral fat decrease of 18.7% (P < 0.001). The total amount of body fat correlated with plasma (serum) leptin before (r = 0.64, P < 0.001) and after (r = 0.75, P < 0.001) weight loss. Plasma leptin concentrations expressed per kg of body fat did not change significantly during weight loss. After controlling for body fat, baseline leptin concentrations were significantly associated with hip circumference (r = 0.57, P < 0.001) but not with any indices of abdominal fat distribution. After weight loss the associations became significant for hip and waist circumference as well as for visceral and abdominal subcutaneous fat. Changes in leptin correlated with changes in all indices of obesity except visceral fat. CONCLUSIONS: Plasma leptin concentrations reflect not only total fat mass but also adipose tissue distribution, especially peripheral fat. Plasma leptin values per kilogram of fat mass do not change significantly with modest weight loss.     

Effect of weight loss on blood pressure changes in overweight patients: A systematic review and meta-analysis

To determine quantitative differences between weight loss and changes in clinic blood pressure (BP) and ambulatory BP in patients with obesity or overweight, the authors performed a meta-analysis. PubMed, Embase, and Scopus databases were searched up to June 2022. Studies that compared clinic or ambulatory BP with weight loss were included. A random effect model was applied to pool the differences between clinic BP and ambulatory BP. Thirty-five studies, for a total of 3219 patients were included in this meta-analysis. The clinic systolic blood pressure (SBP) and diastolic blood pressure (DBP) were significantly reduced by 5.79 mmHg (95% CI, 3.54–8.05) and 3.36 mmHg (95% CI, 1.93–4.75) after a mean body mass index (BMI) reduction of 2.27 kg/m², and the SBP and DBP were significantly reduced by 6.65 mmHg (95% CI, 5.16–8.14) and 3.63 mmHg (95% CI, 2.03–5.24) after a mean BMI reduction of 4.12 kg/m². The BP reductions were much larger in patients with a BMI decrease ≥3 kg/m² than in patients with less BMI decrease, both for clinic SBP [8.54 mmHg (95% CI, 4.62–12.47)] versus [3.83 mmHg (95% CI, 1.22–6.45)] and clinic DBP [3.45 mmHg (95% CI, 1.59–5.30)] versus [3.15 mmHg (95% CI, 1.21–5.10)]. The significant reduction of the clinic and ambulatory BP followed the weight loss, and this phenomenon could be more notable after medical intervention and a larger weight loss.     

Body fat distribution and the prognosis for weight reduction: preliminary observations

In a preliminary study the influence of body fat distribution on the degree of weight reduction, blood lipids and blood glucose was investigated in 17 premenopausal obese women (BMI greater than 27 kg/m2), who followed an energy-reduced diet of 4.2 MJ/day for 8 weeks. Body fat distribution was distinguished in an abdominal and gluteal-femoral type using a cut-off point of 0.80 for the ratio of waist-to-hips girth. Mean weight reduction was about 10 kg. Body fat distribution was not related to the ability to lose weight. Body weight reduction was 10.2 +/- 3.3 kg (mean +/- s.d.) in the abdominal obese (n = 8) and 9.6 +/- 2.4 kg in the gluteal-femoral obese women (n = 8). In abdominal obese women, body fat distribution became more intermediate. This change in body fat distribution coincided in the abdominal obese, after weight loss, with greater decreases in blood glucose and serum lipids than in the gluteal-femoral obese.     

Visceral obesity and the metabolic syndrome: effects of weight loss

A large body of experimental and epidemiological evidence has established an association between visceral obesity and the metabolic syndrome, which retains its power throughout the spectrum of adiposity and is still clinically meaningful in severe obesity. The association may be due to an overload of liver free fatty acids (FFA) produced by the high lipolytic activity of omental fat. A substantial improvement in all aspects of the metabolic syndrome with only a moderate degree of weight loss has been observed in a large number of randomised controlled studies and can also be obtained in severe obesity, despite the fact that the patients remain obese. The reasons for this apparent dissociation between weight loss and metabolic improvement are not yet clearly understood, but may involve the relationship between visceral fat and metabolic alterations. The results of some studies suggest that the favourable metabolic changes observed in obese patients with weight loss may be directly attributable to a reduction in visceral fat, and other studies have recently shown that a rapid and preferential reduction in visceral fat mass occurs during the first phase of weight loss in morbidly obese patients possibly as a result of sympathetic nervous system activation. It is therefore possible that the apparent dissociation between weight loss and metabolic improvement is partially due to a difference in the responsiveness of visceral and subcutaneous adipose tissue to energy restriction: i.e. the fact that the metabolic profile of patients with visceral obesity may substantially improve after the loss of only a few kilograms of body weight could be related to a greater relative reduction in the amount of visceral rather than other fat. In this respect, the characteristically high rate of visceral fat mobilisation can also be seen as a good target for interventions aimed at reducing cardiovascular risk factors.     

Body weight and weight change in relation to blood pressure in normotensive men

We examined blood pressure (BP) in association with weight change since age 20, body mass index (BMI) at different ages and fat distribution in normotensive individuals using baseline survey data collected in the Shanghai Men's Health Study, an ongoing population-based prospective cohort study of Chinese men aged 40-74 years. All anthropometric and BP measurements were performed by medical professionals. Included in this analysis were 25 619 men who had no prior history of hypertension, diabetes or cardiovascular disease, never took any antihypertensive medication and had both normal systolic BP (SBP) and diastolic BP (DBP) (<140/90 mm Hg). Both SBP and DBP increased linearly across the whole range of weight gain since age 20. The adjusted mean differences between the highest and the lowest quintiles of weight gain were 6.0 mm Hg (95% confidence interval (CI): 5.6, 6.5) for SBP and 3.9 (95% CI: 3.6, 4.2) for DBP. When accounting for BMI at age 20, the multivariate-adjusted odds ratio of prehypertension (SBP, 120-139 and/or DBP, 80-89 mm Hg) was 4.1 (95% CI: 3.7, 4.5; P for trend <0.0001) comparing the extreme quintiles of weight gain. Similar positive associations were also observed for BMI at age 40, current BMI, circumferences of the waist and hips and waist-to-hip ratio. In conclusion, these data suggest that weight gain since age 20 and elevated adiposity may contribute significantly to the rise in BP in normotensive individuals, emphasizing the importance of weight control throughout adulthood in preventing high BP.     

Obesity markers and blood pressure in a sample of Portuguese children and adolescents.

BACKGROUND: Little information exists regarding the effect of several obesity markers on blood pressure (BP) levels in youth. DESIGN: Transverse study including 2494 boys and 2589 girls. METHODS: Height, weight and waist were measured according to the international criteria and body fat (BF) by bioimpedance. BP was measured by an automated device. Hypertension was defined using sex-specific, age-specific and height-specific observation-points. RESULTS: Body mass index (BMI) and waist were positively related with systolic blood pressure (SBP) and diastolic blood pressure (DBP) and heart rate in both sexes, whereas the relationships with BF were less consistent. Stepwise linear regression analysis showed that BMI was positively related with SBP and DBP in both sexes, whereas BF was negatively related with SBP in both sexes and with heart rate in boys only; finally, waist was positively related with SBP in boys and heart rate in girls. Age and heart rate-adjusted values of SBP and DBP increased with BMI: for SBP, 117+/-1, 123+/-1 and 124+/-1 mmHg in normal, overweight and obese boys, respectively; corresponding values for girls were 111+/-1, 114+/-1 and 116+/-2 mmHg (mean+/-SE, P<0.001). Overweight and obese boys had an odds ratio for being hypertensive of 2.26 (95% confidence interval: 1.79-2.86) and 3.36 (2.32-4.87), respectively; corresponding values for girls were 1.58 (confidence interval 1.25-1.99) and 2.31 (1.53-3.50). CONCLUSION: BMI, not BF or waist, is consistently and independently related to BP levels in children; overweight and obesity considerably increase the risk of hypertension.     

Obesity and hypertension: long-term effects of weight reduction on blood pressure

Long-term follow-up studies were conducted on massively obese hypertensive subjects during and after a successful protein supplemented fast (PSMF) in order to correlate blood pressure changes with caloric intake and body weight. The blood pressures in 43 subjects were compared during rapid weight loss and at identical weights during post-fast weight gain (Study A). Blood pressures and body weights in 50 subjects were compared prior to starting PSMF and prior to restarting the program 21 months later (Study B). One hundred twenty-five compliant subjects were observed after one month of weight maintenance (Study C-1), and 39 subjects were followed during six months of weight maintenance (Study C-2). In Study A, during subsequent weight gain on an unrestricted diet blood pressure was significantly higher than at identical weight during continuous weight loss on PSMF. However, this increase in blood pressure was only approximately 30 percent of the original decrease. In Study B, weight loss and blood pressure reduction were significantly correlated. After one month of weight maintenance following continuous weight loss of 73 lb, there was no increase in blood pressure (Study C-1). A small but significant increase in blood pressure after six months (Study C-2) was associated with similar small weight increment. However, all blood pressures remained well within the normotensive range and significantly lower than control values. In this study, long-term changes in blood pressure correlated with changes in body weight.     

Efficacy and safety of sibutramine for weight loss in obese patients with hypertension well controlled by beta-adrenergic blocking agents: a placebo-controlled, double-blind, randomised trial

Sibutramine is a serotonin-noradrenaline reuptake inhibitor that is effective for long-term weight reduction and maintenance in obese patients when used as an adjunct to dietary and behavioural measures. Because the inhibition of noradrenaline reuptake may be expected to increase systolic and diastolic blood pressure (SBP and DBP) and pulse rate (PR), a 12-week multi-centre, placebo-controlled, double-blind study was designed to evaluate the efficacy and tolerability of sibutramine for weight loss in obese patients whose hypertension was well controlled (DBP < or = 95 mm Hg) by beta-adrenergic blocking agents (beta-blockers), with or without concomitant thiazide diuretics. Of the 61 patients randomised to sibutramine 20 mg once daily or placebo, 55 patients (90%) completed the study. After 12 weeks, sibutramine-treated patients lost significantly more weight than placebo-treated patients: mean weight reductions were 4.2 kg (4.5%) in the sibutramine group vs 0.3 kg (0.4%) in the placebo group (P<0.001). Greater weight reduction on sibutramine was accompanied by trends for greater mean reductions in serum triglycerides and very low density lipoprotein cholesterol. Sibutramine was well tolerated, and most adverse events were mild or moderate in severity. No sibutramine patient discontinued treatment because of an adverse event. Mean supine and standing DBP and SBP were not statistically significantly different between the sibutramine group and the placebo group at any post-baseline visit during the 12-week trial. At week 12, mean increases from baseline supine SBP and DBP, respectively, were 1.6 and 1.7 mm Hg for the sibutramine group vs increases of 0.4 and 1.3 mm Hg for the placebo group. At week 12, mean increases from baseline standing SBP and DBP, respectively, were 1.5 and 1.8 mm Hg for the sibutramine group vs an increase of 0.3 and a decrease of 0.8 mm Hg for the placebo group (P > 0.05 for treatment comparison). A statistically significant mean increase of 5.6 bpm (+/-8.25, s.d.) in supine PR from a baseline of 62 bpm was reported in sibutramine-treated patients at week 12, whereas placebo-treated patients had a mean supine PR decrease of 2.2 bpm (+/-6.43) (P < 0.001). In summary, sibutramine was well tolerated and effective in weight reduction. The addition of sibutramine did not result in an increase in BP in obese patients whose hypertension was well controlled by a beta-blocker. However, based on the potential for changes in BP and PR, obese patients being treated with sibutramine should be monitored periodically for changes in BP and PR and managed appropriately.     

Effects of weight loss after bariatric surgery on epicardial fat measured using echocardiography

Epicardial fat assessed using echocardiography is associated with abdominal visceral adipose tissue and cardiovascular risk factors. Because of its location, epicardial fat may directly affect the coronary vasculature and myocardium through local secretion of bioactive molecules. This study examines the effects of weight loss after bariatric surgery on epicardial adipose tissue in patients with severe obesity. Clinical data and echocardiograms of 23 patients with severe obesity who had echocardiograms recorded before and 8.3 +/- 3.7 months after undergoing bariatric surgery were retrospectively reviewed. Epicardial fat thickness was measured as the hypoechoic space anterior to the right ventricle in both the parasternal long- and short-axis views, and an average was obtained. At baseline, patients had increased epicardial fat compared with normal-weight controls matched for age, gender, and ethnicity (5.3 +/- 2.4 vs 3.0 +/- 1.1 mm, p <0. 001). Epicardial fat thickness was associated with the patient's initial weight in severely obese patients (r = 0.51, p = 0.011). Patients lost an average of 40 +/- 14 kg after surgery. Epicardial fat thickness decreased from 5.3 +/- 2.4 to 4.0 +/-1.6 mm (p = 0.001). Change in epicardial fat correlated with initial epicardial fat thickness measured using echocardiography (r = 0.71, p <0.001). In conclusion, epicardial fat thickness decreases in severely obese patients who have substantial weight loss after bariatric surgery. Measuring epicardial fat thickness using echocardiography may be useful to monitor visceral fat loss with weight reduction therapies.     

Changes in blood pressure and body weight following smoking cessation in women

OBJECTIVE: Few have studied the long-term effects of smoking and smoking cessation on weight gain and blood pressure increase and compared with the age-related increases experienced by most adults. This study compared the development of weight and blood pressure in female never smokers, continuing smokers and smokers who quit smoking. DESIGN: Weight, systolic (SBP) and diastolic (DBP) blood pressure and smoking habits were assessed at baseline and re-assessed after a mean follow-up of 9.0 +/- 5.8 years. SETTING: Population-based cohort. SUBJECTS: A total of 2381 female never smokers and 1550 female smokers. At the re-examination, 388 of the smokers had quit smoking. RESULTS: Mean weight gain was 7.6 +/- 6.1, 3.2 +/- 5.8 and 3.7 +/- 5.2 kg, respectively, in quitters, continuing smokers and never smokers (P < 0.001). In women without blood pressure treatment, mean SBP increase was 20.9 +/- 16.8, 19.1 +/- 15.8 and 16.1 +/- 16.3 mmHg, respectively, in these groups (P < 0.001). Mean DBP increase was 6.2 +/- 8.7, 5.7 +/- 9.3 and 3.1 +/- 8.0 mmHg, respectively (P < 0.001). After adjustments for potential confounders, the increased weight gain in quitters remained highly significant. The differences in SBP and DBP increase were attenuated after adjustments, but remained significant. Incidence of hypertension (> or = 160/95 mmHg or treatment) was significantly higher in quitters [adjusted odds ratio (OR): 1.8; CI: 1.4-2.5] when compared with continuing smokers (OR: 1.3; CI: 1.07-1.6) and never smokers (reference). CONCLUSION: Over a long follow-up, weight gain was approximately 3-4 kg higher in quitters when compared with continuing smokers or never smokers. Although the differences in blood pressure increase were moderate, smoking cessation was associated with an increased incidence of hypertension.     

Association between basal serum and leptin levels and changes in abdominal fat distribution during weight loss

The aim of this study was to evaluate the relationship between changes in abdominal fat areas and the baseline serum leptin levels of Japanese obese women during weight reduction. The study was performed on 100 obese female Japanese volunteers. We measured the BMI and abdominal fat areas (visceral, subcutaneous and total) by magnetic resonance imaging and determined the fasting serum leptin levels before and after a 3 month weight reduction program. We examined whether or not a relationship exists between the baseline leptin levels and the subsequent changes in the abdominal fat areas after a weight reduction program. Multiple linear regression analysis was performed to examine the relationship between the baseline leptin levels and changes in abdominal visceral, subcutaneous, and total fat areas, and demonstrated that the baseline leptin level was a significant predictive factor for changes in the abdominal visceral fat area in both pre and postmenopausal Japanese obese women. We thus concluded the relatively higher baseline leptin levels in Japanese obese women to be associated with a relatively smaller reduction in the amount of abdominal visceral fat after undergoing a weight reduction program.     

Relationship among systolic blood pressure, serum insulin and leptin, and visceral fat accumulation in obese children.

The aim of this study was to clarify the relation among systolic blood pressure (SBP), serum insulin, leptin, visceral fat accumulation and family history of hypertension, and to elucidate the pathophysiologic mechanism of blood pressure elevation in obese children. This study examined 109 obese children with a family history of hypertension (OF: 77 boys and 32 girls), and 83 obese children without such a history (ON: 60 boys and 23 girls). Body height and weight, and percent of body fat were measured and the percent of relative weight was calculated. Both boys and girls, the two groups were matched with respect to age, height, and weight. SBP was measured in the seated position using an automated recorder. Abdominal fat thickness (maximum preperitoneal fat thickness: Pmax; minimum subcutaneous fat thickness: Smin) were measured using ultrasonography. The fasting serum levels of insulin and leptin were measured by radioimmunoassay. All subjects were simply obese, without diabetic states. In both OF and ON, SBP was associated with insulin levels, leptin levels, and Pmax by simple regression analysis, and with insulin levels by stepwise regression analysis. Insulin levels were associated with leptin levels and Pmax by simple regression analysis, and with leptin levels by stepwise regression analysis. These findings indicated that SBP was associated with hyperinsulinemia, hyperleptinemia and visceral accumulation regardless of a family history of hypertension in obese children, as well as later in adult obesity. For primary prevention of hypertension, these results support the importance of implementation of a strategy to prevent obesity, especially visceral obesity. An effective strategy for preventing childhood obesity will contribute to a future decrement in cases of metabolic syndrome, including adulthood hypertension.     

Effect of weight reduction on serum ghrelin and TNFalpha concentrations in obese women

Background: Ghrelin causes weight gain by increasing food intake in rodents. Tumor necrosis factor alpha (TNFalpha) is produced by adipose tissue, modulates its metabolism and stimulates catabolic processes. The aim of our study was to evaluate whether weight loss treatment modulates serum concentrations of TNFalpha and ghrelin in obese women. Methods: The study groups included 46 women: 35 obese patients and 11 controls. Serum concentrations of ghrelin and TNFalpha were measured by ELISA before and after a 3-month weight reduction treatment that consisted of a 1000 kcal/day diet and physical exercises. Body composition was determined by impedance analysis using Bodystat. Results: There were no differences in plasma ghrelin concentrations between obese patients and controls. TNFalpha serum levels were higher in obese patients than in controls (p=0.000). The mean weight loss over the 3-month treatment period was 8.7+/-4.5 kg. Following weight loss, serum ghrelin concentration increased significantly (66.3+/-13.7 vs. 73.7+/-14.8 pg/ml; p=0.002) and TNFalpha concentrations decreased significantly (6.9+/-2.6 vs. 5.2+/-1.5 pg/ml; p=0.002). Ghrelin did not show a correlation with weight or percentage of body fat. There was a positive correlation between the increase in ghrelin and the decrease in body fat percentage during weight loss (p=0.002). Conclusion: The increase in serum ghrelin and the decrease in serum TNFalpha, as observed after weight reduction treatment in obese subjects, may constitute a counter-regulatory mechanism preventing further weight loss.     

A dietary fibre supplement and weight maintenance after weight reduction: a randomized, double-blind, placebo-controlled long-term trial

Ninety-seven mildly obese females (BMI = 27.4 kg/m2) were in a randomized, double-blind, placebo-controlled trial treated for 52 weeks. The treatment consisted of a hypocaloric diet providing 5000 kJ/day (1200 kcal) and a dietary fibre supplement of 7 g/day for 11 weeks, (part I), followed by a diet providing 6720 kJ/day (1600 kcal) and a dietary fibre supplement of 6 g/day for 16 weeks (part II). Finally placebo was withdrawn and all still adhering subjects were given a dietary fibre supplement of 6 g/day and an ad libitum diet for the rest of the period (part III). Initial body weights were comparable, 76.9 +/- 0.8 kg in the fibre group versus 77.7 +/- 1.3 kg in the placebo group. During part I the weight reduction in the fibre group of 4.9 kg was significantly higher compared to that of 3.3 kg in the placebo group (P = 0.05). Accumulated weight reduction during part II was still significantly higher in the fibre group, 3.8 kg, compared to 2.8 kg in the placebo group (P less than 0.05). Total weight loss in the fibre group after 52 weeks was 6.7 kg. Probability of adherence to the treatment regimen was significantly higher in the fibre group from week 13 and onwards (P less than 0.01). Initial blood pressures were comparable. A significant reduction of systolic blood pressure occurred in both groups. A significant reduction of diastolic blood pressure occurred in the fibre group only, from 85.4 +/- 1.2 mmHg to 81.7 +/- 1.1 mmHg (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

人体质量指数与运动血压的相关性研究

目的：观察人体质量指数（BMI）不同的患者行平板运动试验时运动血压的变化。方法：BMI正常患者224例（正常对照组）,肥胖患者109例（肥胖组）,行平板运动实验检查,比较两组之间运动血压的差别,并分析BMI和运动血压之间的相关性。结果：肥胖组患者静息血压（收缩压、舒张压）,运动峰值血压（收缩压、舒张压）,恢复期血压（收缩压、舒张压）和恢复期脉压均明显高于正常对照组（P〈0.05）。肥胖组患者运动高血压的发生率明显高于正常对照组（9.2%比3.6%,P〈0.05）,且BMI与运动血压呈明显正相关（r=0.123～0.205,P〈0.05）。结论：肥胖患者运动中血压变化异常,提示肥胖患者有血管舒缩功能障碍和心脏自主神经功能紊乱。     

Ambulatory blood pressure monitoring in obese children: role of insulin resistance

OBJECTIVES: To investigate the relationship between ambulatory blood pressure (ABPM) parameters and insulin resistance in obese children. METHODS: A population of 56 obese prepubertal children was recruited for the study. They underwent ABPM, an oral glucose tolerance test and complete physical examination, including adiposity indexes such as body mass index (BMI), skinfolds, waist-to-hip ratio (WHR) and fat mass. RESULTS: The standard deviation score for BMI was significantly correlated with 24-h systolic blood pressure (SBP) (r = 0.30; P = 0.02) and diastolic blood pressure (DBP) (r = 0.29; P = 0.03), daytime SBP and DBP (r = 0.28; P = 0.04 and r = 0.32; P = 0.02), night-time SBP and DBP (r = 0.32; P = 0.01 and r = 0.27; P = 0.04). Fat mass was correlated with 24-h SBP (r = 0.46; P = 0.005), daytime SBP (r = 0.40; P = 0.01) and night-time SBP (r = 0.49; P = 0.03). No correlations were found between ABPM parameters and WHR. Furthermore, significant correlations were found between insulin resistance indexes, such as the homeostasis model assessment of insulin resistance and quantitative insulin-sensitivity check index, and 24-h DBP (r = 0.34; P = 0.01 and r = -0.29; P = 0.03), daytime DBP (r = 0.35; P = 0.009 and r = -0.34; P = 0.01) and daytime SBP (r = 0.32; P = 0.02 and r = -0.27; P = 0.04). Only 24-h and daytime DBP remained correlated with insulin resistance after adjustment for obesity. The analysis of the circadian rhythm of blood pressure revealed that 24 out the 56 children were non-dippers. CONCLUSIONS: The results of the present study indicate that adiposity and insulin resistance have an important role in influencing blood pressure in obese children, and also show a high prevalence of non-dipping phenomenon. This is of particular relevance because blood pressure tracks from childhood into adulthood and an already early-life high blood pressure is associated with an increased cardiovascular risk.