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Background/Objectives: In spite of the much evidence for the beneficial effects of probiotics, their anti-obesity effects have not been well examined. We evaluated the effects of the probiotic Lactobacillus gasseri SBT2055 (LG2055) on abdominal adiposity, body weight and other body measures in adults with obese tendencies. Subjects/Methods: We conducted a multicenter, double-blind, randomized, placebo-controlled intervention trial. Subjects (n=87) with higher body mass index (BMI) (24.2–30.7 kg/m2) and abdominal visceral fat area (81.2–178.5 cm2) were randomly assigned to receive either fermented milk (FM) containing LG2055 (active FM; n=43) or FM without LG2055 (control FM; n=44), and were asked to consume 200 g/day of FM for 12 weeks. Abdominal fat area was determined by computed tomography. Results: In the active FM group, abdominal visceral and subcutaneous fat areas significantly (P<0.01) decreased from baseline by an average of 4.6% (mean (confidence interval): −5.8 (−10.0, −1.7) cm2) and 3.3% (−7.4 (−11.6, −3.1) cm2), respectively. Body weight and other measures also decreased significantly (P<0.001) as follows: body weight, 1.4% (−1.1 (−1.5, −0.7) kg); BMI, 1.5% (−0.4 (−0.5, −0.2) kg/m2); waist, 1.8% (−1.7 (−2.1, −1.4) cm); hip, 1.5% (−1.5 (−1.8, −1.1) cm). In the control group, by contrast, none of these parameters decreased significantly. High-molecular weight adiponectin in serum increased significantly (P<0.01) in the active and control groups by 12.7% (0.17 (0.07, 0.26) μg/ml) and 13.6% (0.23 (0.07, 0.38) μg/ml), respectively. Conclusion: The probiotic LG2055 showed lowering effects on abdominal adiposity, body weight and other measures, suggesting its beneficial influence on metabolic disorders.

Consumption of fermented milk (FM) containing a probiotic, Lactobacillus gasseri SBT2055 (LG2055), previously showed a reduction in abdominal adiposity in a randomised controlled trial (RCT) using FM with 108 colony-forming units (cfu) of LG2055/g. However, whether the effectiveness is observed at lower concentrations, the recommended minimum or intermediate levels of probiotics (106 or 107cfu/g, respectively), remains to be examined. A multi-centre, double-blind, parallel-group RCT was conducted using 210 healthy Japanese adults with large visceral fat areas (80·2–187·8 cm2). They were balanced for their baseline characteristics and randomly assigned to three groups receiving FM containing 107, 106 or 0 (control) cfu LG2055/g of FM, and were asked to consume 200 g FM/d for 12 weeks. Abdominal visceral fat areas, which were determined by computed tomography, at week 12, changed from baseline by an average of − 8·5 % (95 % CI − 11·9, − 5·1; P< 0·01) in the 107 dose group, and by − 8·2 % (95 % CI − 10·8, − 5·7; P< 0·01) in the 106 dose group. Other measures including BMI, waist and hip circumferences, and body fat mass were also significantly decreased from baseline at week 12 in both groups; interestingly, the cessation of taking FM for 4 weeks attenuated these effects. In the control group, none of these parameters significantly decreased from baseline. These findings demonstrate that consumption of LG2055 at doses as low as the order of 108cfu/d exhibited a significant lowering effect on abdominal adiposity, and suggest that constant consumption might be needed to maintain the effect.

Lactoferrin (LF), a multifunctional glycoprotein in mammalian milk, is reported to exert a modulatory effect on lipid metabolism. The aim of the present study was to elucidate whether enteric-coated LF (eLF) might improve visceral fat-type obesity, an underlying cause of the metabolic syndrome. Using a double-blind, placebo-controlled design, Japanese men and women (n 26; aged 22–60 years) with abdominal obesity (BMI>25 kg/m2, and visceral fat area (VFA)>100 cm2) consumed eLF (300 mg/d as bovine LF) or placebo tablets for 8 weeks. Measurement of the total fat area, VFA and subcutaneous fat area from computed tomography images revealed a significant reduction in VFA ( − 14·6 cm2) in the eLF group, as compared with the placebo controls ( − 1·8 cm2; P = 0·009 by ANCOVA). Decreases in body weight, BMI and hip circumference in the eLF group ( − 1·5 kg, − 0·6 kg/m2, − 2·6 cm) were also found to be significantly greater than with the placebo (+1·0 kg, +0·3 kg/m2, − 0·2 cm; P = 0·032, 0·013, 0·041, respectively). There was also a tendency for a reduction in waist circumference in the eLF group ( − 4·4 cm) as compared with the placebo group ( − 0·9 cm; P = 0·073). No adverse effects of the eLF treatment were found with regard to blood lipid or biochemical parameters. From these results, eLF appears to be a promising agent for the control of visceral fat accumulation.

Hibiscus sabdariffa L. (HS) has been investigated as an alternative treatment for metabolic syndrome (MetS), as it affects all MetS components with low side effects simultaneously; however, clinical evidence regarding its efficacy compared with placebo is inconsistent. This study assessed how the aqueous calyx extract of HS influences insulin resistance and MetS parameters and examined the safety effects on liver, kidney, and hematological indexes in participants with abdominal obesity and mild MetS symptoms. In this double-blind, randomized, placebo-controlled trial, 108 participants with MetS were randomly assigned to take 1000-mg HS (45.04 mg/day in total polyphenols) or placebo daily for 12 weeks. Insulin resistance (HOMA-IR), glycemic markers, body mass index (BMI), waist circumference (WC), lipid profiles, and blood pressure were assessed at baseline, 6 weeks, and 12 weeks. Additionally, liver and kidney function indicators along with hematological parameters were evaluated. Compared with placebo, HS did not significantly affect HOMA-IR, glycemic markers, BMI, WC, lipid profile, or blood pressure. Although HS did not significantly alter the lipid profile overall, serum low-density lipoprotein (LDL) levels decreased significantly at 12 weeks compared with baseline (− 7.98 mg/dL, [95 % CI, − 14.80, − 1.15]). Additionally, HS did not cause significant liver or kidney function or hematological changes compared with placebo. Taking 1000-mg HS daily for 12 weeks seems to be safe. Placebo and HS groups showed good clinical results, and the extract was not associated with improved metabolic parameters in individuals with abdominal obesity and mild MetS symptoms, with the exception of lower serum LDL. •Hibiscus sabdariffa L (HS) is safe and without severe side effects.•HS exhibited a significant reduction in serum LDL levels compared to baseline.•HS did not affect insulin resistance, body mass index, and waist circumference.•This study conducted stratified block randomization by body mass index.

ObjectiveThe aim of this trial was to determine whether obese patients benefit from treatment with rimonabant in terms of progression of carotid atherosclerosis. Rimonabant, a selective cannabinoid-1 receptor blocker, reduces body weight and improves cardiometabolic risk factors in patients who are obese.Design, setting, patients, interventions and resultsA prospective, double-blind, placebo-controlled trial (Atherosclerosis Underlying Development assessed by Intima–media Thickness in patients On Rimonabant (AUDITOR)) randomised 661 patients with abdominal obesity and metabolic syndrome to rimonabant or placebo for 30 months of treatment. The absolute change in the average value for six segments of far wall carotid intima–media thickness from baseline to month 30 was 0.010±0.095 mm in the rimonabant group and 0.012±0.091 mm in the placebo group (p=0.67). The annualised change was an increase of 0.005±0.042 mm for the rimonabant-treated group and 0.007±0.043 mm for the placebo-treated group (p=0.45).ConclusionsThere was no difference in atherosclerosis progression between patients receiving rimonabant for 30 months and those receiving placebo for the primary efficacy measure (absolute change in carotid intima–media thickness). These findings are consistent with a similar study using coronary intravascular ultrasound and another study evaluating the occurrence of cardiovascular events. Our findings suggest that a 5% loss of body weight over a 30-month period with rimonabant is insufficient to modify atherosclerosis progression in the carotid artery in obese patients with metabolic syndrome.Clinical trial registration informationclinicaltrials.gov Identifier: NCT00228176.

In China, most normal BMI (body mass index of ≥18.5 to <25 kg/m2) adults with type 2 diabetes (T2DM) exhibit visceral adiposity. This study compared the effects of exenatide and humalog Mix25 on normal BMI patients with T2DM and visceral adiposity. A total of 95 patients were randomized to receive either exenatide or humalog Mix25 treatment for 24 weeks. Subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) were quantified by magnetic resonance imaging (MRI) and liver fat content (LFC) by liver proton magnetic resonance spectroscopy (1H MRS). Each patient’s weight, waist circumference, BMI, blood glucose, insulin sensitivity, pancreatic β-cell function, and fibroblast growth factor 21 (FGF-21) levels were measured. Data from 81 patients who completed the study (40 and 41 in the exenatide and humalog Mix25 groups, respectively) were analysed. The change in 2 h plasma blood glucose was greater in the exenatide group (P=0.039). HOMA-IR and MBCI improved significantly after exenatide therapy (P<0.01, P=0.045). VAT and LFC decreased in both groups (P<0.01 for all) but to a greater extent in the exenatide group, while SAT only decreased with exenatide therapy (P<0.01). FGF-21 levels declined more in the exenatide group (P<0.01), but were positively correlated with VAT in the entire cohort before (r=0.244, P=0.043) and after (r=0.290, P=0.016) the intervention. The effects of exenatide on glycaemic metabolism, insulin resistance, pancreatic β-cell function, and fat deposition support its administration to normal BMI patients with T2DM and visceral adiposity.

Fenofibrate is a peroxisome proliferator-activated receptor-α that has been clinically used to treat dyslipidemia and insulin resistance. To better understand the molecular mechanisms underlying fenofibrate action, we investigated whether fenofibrate affects serum levels of vaspin, an adipocytokine that has recently been shown to link obesity and insulin resistance. Fenofibrate treatment significantly increased serum vaspin levels of dyslipidemic patients, which correlated with reduced body weight and increased insulin sensitivity. To elucidate the biochemical mechanisms of fenofibrate action, we investigated the effect of fenofibrate on vaspin mRNA and protein expressions in obese rats. Fenofibrate greatly increased vaspin mRNA and protein levels in visceral adipose tissue consisting of retroperitoneal, mesenteric, and periepididymal adipose tissue but not in the subcutaneous adipose tissue, which correlated with increased serum vaspin levels and increased insulin sensitivity in obese rats. Consistent with a direct effect on vaspin expression, fenofibrate treatment significantly increased the mRNA and protein expression levels of vaspin in 3T3-L1 adipocytes. Together, our results demonstrate for the first time that fenofibrate upregulates vaspin expression in dyslipidemic human subjects and suggest that upregulation of vaspin expression in adipocytes may provide a mechanism by which fenofibrate improves insulin sensitivity in dyslipidemic patients.

In previous studies, abdominal obesity has been related to total low-grade inflammation and in some cases has resulted in insulin resistance and other metabolism related disorders such as diabetes. Quercetin is a polyphenol, which is a derivative of plants, and has been shown in vitro as well as in a few animal models to have several potential anti-inflammatory as well as anticarcinogenic applications. The substance has also been shown to aid in the attenuation of lipid peroxidation, platelet aggregation, and capillary permeability. However, further research is called for to gain a better understanding of how quercetin is able to provide these beneficial effects. This manuscript reviewed quercetin’s anti-inflammatory properties in relation to obesity and type 2 diabetes.

Background: Risk factors for obstructive sleep apnea (OSA) are male gender, obesity and abnormalities in neck soft tissue mass. OSA is associated with both growth hormone (GH) excess and severe GH deficiency in adults. Adults with abdominal obesity have markedly suppressed GH secretion. Aim: To study the effect of GH treatment on OSA in abdominally obese men with impaired glucose tolerance. Patients and Methods: Forty men with abdominal obesity and glucose intolerance were randomized in a prospective, 12-month double-blind trial to receive either GH or placebo. The treatment groups had similar BMI and waist circumference. Overnight polysomnography and computed tomography to assess muscle and fat distribution in the neck and abdomen were performed at baseline and after 12 months. Results: GH treatment increased insulin-like growth-factor-1 from (mean [SD]) 168 (72) to 292 (117) μg/L, the apnea-hypopnea index from (n/h) 31 (20) to 43 (25) and oxygen-desaturation index from (n/h) 18 (14) to 29 (21) (p = 0.0001, 0.001, 0.002). Neck transverse diameter, circumference and total cross-sectional area (p = 0.007, 0.01, 0.02) increased, while abdominal visceral adipose tissue (p = 0.007) was reduced. No between-group differences in total sleep time, REM sleep, NREM sleep, and time spent in supine position were found. The Epworth sleepiness scale score was unchanged. Conclusions: GH treatment increased the severity of OSA in abdominally obese men. The possible mechanism appears to be reflected by the GH-induced increase of measures of neck volume. The present results, to some extent, argue against that low GH/IGF-I activity is a primary cause of OSA in abdominally obese men. Citation: Karimi M; Koranyi J; Franco C; Peker Y; Eder DN; Angelhed JE; Löonn L; Grote L; Bengtsson BA; Svensson J: Hedner J; Johannsson G. Increased neck soft tissue mass and worsening of obstructive sleep apnea after growth hormone treatment in men with abdominal obesity. J Clin Sleep Med 2010;6(3):256–263.

The association between obesity, cancer and cardiovascular disease (CVD) has been demonstrated in animal and epidemiological studies. However, the specific role of visceral obesity on cancer and CVD remains unclear. Visceral adipose tissue (VAT) is a complex and metabolically active tissue, that can produce different adipokines and hormones, responsible for endocrine-metabolic comorbidities. This review explores the potential mechanisms related to VAT that may also be involved in cancer and CVD. In addition, we discuss the shared pharmacological treatments which may reduce the risk of both diseases. This review highlights that chronic inflammation, molecular aspects, metabolic syndrome, secretion of hormones and adiponectin associated to VAT may have synergistic effects and should be further studied in relation to cancer and CVD. Reductions in abdominal and visceral adiposity improve insulin sensitivity, lipid profile and cytokines, which consequently reduce the risk of CVD and some cancers. Several medications have shown to reduce visceral and/or subcutaneous fat. Further research is needed to investigate the pathophysiological mechanisms by which visceral obesity may cause both cancer and CVD. The role of visceral fat in cancer and CVD is an important area to advance. Public health policies to increase public awareness about VAT’s role and ways to manage or prevent it are needed.