Obesity-related Metabolic Syndrome Research Articles

Epidemiological Evidences for the Association of Obesity and Metabolic Disorders with Oral Diseases

Obesity is the underlying cause of many chronic diseases and affects overall health. Obesity and obesity-related metabolic disorders, particularly, metabolic syndrome and diabetes, have been recognized to be associated with oral diseases. This review describes the recent evidence from epidemiological studies investigating the effect of obesity and metabolic disorders on oral diseases, including dental caries and periodontal disease in adults. Longitudinal studies indicate the direction of association that obesity and diabetes affect periodontal disease. Interpretation of causal relationships between metabolic syndrome and periodontal disease remains limited because of the small number of prospective evidence. Longitudinal studies investigating dental caries have not been performed. Further exploration of the effect of metabolic syndrome on periodontal disease, and that of obesity and metabolic disorders on dental caries in longitudinal studies, is warranted.

Anti-Obesity and Anti-Diabetic Effect of Neoagarooligosaccharides on High-Fat Diet-Induced Obesity in Mice.

Neoagarooligosaccharides (NAOs), mainly comprising neoagarotetraose and neoagarohexaose, were prepared by hydrolyzing agar with β-agarase DagA from Streptomyces coelicolor, and the anti-obesity and anti-diabetic effects of NAOs on high-fat diet (HFD)-induced obesity in mice were investigated after NAOs-supplementation for 64 days. Compared to the HFD group, the HFD-0.5 group that was fed with HFD + NAOs (0.5%, w/w) showed remarkable reduction of 36% for body weight gain and 37% for food efficiency ratios without abnormal clinical signs. Furthermore, fat accumulation in the liver and development of macrovesicular steatosis induced by HFD in the HFD-0.5 group were recovered nearly to the levels found in the normal diet (ND) group. NAOs intake could also effectively reduce the size (area) of adipocytes and tissue weight gain in the perirenal and epididymal adipose tissues. The increased concentrations of total cholesterol, triglyceride, and free fatty acid in serum of the HFD group were also markedly ameliorated to the levels found in serum of the ND group after NAOs-intake in a dose dependent manner. In addition, insulin resistance and glucose intolerance induced by HFD were distinctly improved, and adiponectin concentration in the blood was notably increased. All these results strongly suggest that intake of NAOs can effectively suppress obesity and obesity-related metabolic syndromes, such as hyperlipidemia, steatosis, insulin resistance, and glucose intolerance, by inducing production of adiponectin in the HFD-induced obese mice.

Chondroitin Sulfate Inhibits Monocyte Chemoattractant Protein-1 Release From 3T3-L1 Adipocytes: A New Treatment Opportunity for Obesity-Related Inflammation?

Monocyte chemoattractant protein-1 (MCP-1) overproduction from inflamed adipose tissue is a major contributor to obesity-related metabolic syndromes. 3T3-L1 embryonic fibroblasts were cultured and differentiated into adipocytes using an established protocol. Adipocytes were treated with lipopolysaccharide (LPS) to induce inflammation and thus MCP-1 release. At the same time, varying concentrations of chondroitin sulfate (CS) were added in a physiologically relevant range (10-200 µg/mL) to determine its impact on MCP-1 release. Chondroitin sulfate, a natural glycosaminoglycan of connective tissue including the cartilage extracellular matrix, was chosen on the basis of our previous studies demonstrating its anti-inflammatory effect on macrophages. Because the main action of MCP-1 is to induce monocyte migration, cultured THP-1 monocytes were used to test whether CS at the highest physiologically relevant concentration could inhibit cell migration induced by human recombinant MCP-1. Chondroitin sulfate (100-200 µg/mL) inhibited MCP-1 release from inflamed adipocytes in a dose-dependent manner (P < .01, 95% confidence interval [CI]: −5.89 to −3.858 at 100 µg/mL and P < .001, 95% CI: −6.028 to −3.996 at 200 µg/mL) but had no effect on MCP-1–driven chemotaxis of THP-1 monocytes. In summary, CS could be expected to reduce macrophage infiltration into adipose tissue by reduction in adipocyte expression and release of MCP-1 and as such might reduce adipose tissue inflammation in response to pro-inflammatory stimuli such as LPS, now increasingly recognized to be relevant in vivo.

5,7-Dimethoxyflavone Attenuates Obesity by Inhibiting Adipogenesis in 3T3-L1 Adipocytes and High-Fat Diet-Induced Obese C57BL/6J Mice.

The antiobesity effect of 5,7-dimethoxyflavone (DMF) was evaluated in 3T3-L1 adipocytes and high-fat diet (HFD)-induced obese C57BL/6J mice. The accumulation of lipid droplets and triglycerides in adipocytes was dose dependently suppressed by DMF through inhibition of adipogenesis. DMF downregulated the adipogenic transcription factors (peroxisome proliferator-activated receptor [PPAR]γ, CCAAT/enhancer binding protein [C/EBP]α, and sterol regulatory element-binding protein-1c [SREBP-1c]) and lipid synthesis enzymes (fatty acid synthase [FAS], acetyl-CoA carboxylase [ACC], lipoprotein lipase [LPL], and HMG-CoA reductase [HMGR]). AMP-activated protein kinase (AMPK) and AMPK related lipolytic proteins in differentiated adipocytes were activated by DMF. In the animal model, oral administration of DMF (50 mg/kg/day for 6 weeks) significantly decreased body weight gain without affecting food intake. Elevated serum levels of total cholesterol and low-density lipoprotein cholesterol were suppressed by DMF. Fat pad masses were reduced in DMF-treated obese mice, as evidenced by reduced adipocyte size. DMF altered the expression of adipogenic transcription factors in epididymal fat tissue. In addition, DMF attenuated HFD-induced nonalcoholic fatty liver disease by decreasing hepatic triglyceride accumulation. Overall, these results suggest that DMF is a potential natural agent for attenuating obesity and other obesity-related metabolic syndromes.

Diet-induced obesity skin changes monitored by in vivo SHG and ex vivo CARS microscopy.

Obesity related metabolic syndrome and type 2 diabetes have severe consequences on our skin. Latest developments in nonlinear microscopy allow the use of noninvasive, label free imaging methods, such as second harmonic generation (SHG) and coherent anti-Stokes Raman scattering (CARS), for early diagnosis of metabolic syndrome-related skin complications by 3D imaging of the skin and the connective tissue. Our aim was to study effects of various types of diet-induced obesity in mice using these methods. We examined mice on different diets for 32 weeks. The collagen morphology was evaluated four times in vivo by SHG microscopy, and adipocytes were examined once at the end of experiment by ex vivo CARS method. A strong correlation was found between the body weight and the adipocyte size, while we found that the SHG intensity of dermal collagen reduces considerably with increasing body weight. Obese mice on high-fat diet showed worse results than those on high-fat - high-fructose diet. Animals on high-fructose diet did not gain more weight than those on ordinary diet despite of the increased calorie intake, but their collagen damage was nonetheless significant. Obesity and high sugar intake damages the skin, mainly the dermal connective tissue and subcutaneous adipose tissue, which efficiently can be monitored by in vivo SHG and ex vivo CARS microscopy.

Is Synovial Macrophage Activation the Inflammatory Link Between Obesity and Osteoarthritis?

Osteoarthritis (OA) is the most common musculoskeletal disease, affecting nearly 25% of the world population(WHO reports), leading to pain and disability. There are as yet no clinically proven therapies to halt OA onset or progression; the development of such therapies is, therefore, a national as well as international research priority. Obesity-related metabolic syndrome has been identified as the most significant, but also an entirely preventable risk factor for OA; however, the mechanisms underlying this link remain unclear. We have examined the available literature linking OA and metabolic syndrome. The two conditions have a shared pathogenesis in which chronic low-grade inflammation of affected tissues is recognized as a major factor that is associated with systemic inflammation. In addition, the occurrence of metabolic syndrome appears to alter systemic and local pro-inflammatory cytokines that are also related to the development of OA-like pathologies. Recent findings highlight the importance not only of the elevated number of macrophage in inflamed synovium but also the activation and amplification of the inflammatory state and other pathological changes. The role of local inflammation on the synovium is now considered to be a pharmacological target against which to aim disease-modifying drugs. In this review, we evaluate evidence linking OA, synovitis and metabolic syndrome and discuss the merits of targeting macrophage activation as a valid treatment option for OA.

NONALCOHOLIC FATTY LIVER DISEASE BRAZILIAN SOCIETY OF HEPATOLOGY CONSENSUS.

The prevalence of obesity-related metabolic syndrome has rapidly increased in Brazil, resulting in a high frequency of nonalcoholic fatty liver disease, that didn't receive much attention in the past. However, it has received increased attention since this disease was identified to progress to end-stage liver diseases, such as cirrhosis and hepatocellular carcinoma. Clinical practice guidelines for the diagnosis and treatment of nonalcoholic fatty liver disease have not been established in Brazil. The Brazilian Society of Hepatology held an event with specialists' members from all over Brazil with the purpose of producing guideline for Nonalcoholic Fatty Liver Disease based on a systematic approach that reflects evidence-based medicine and expert opinions. The guideline discussed the following subjects: 1-Concepts and recommendations; 2-Diagnosis; 3-Non-medical treatment; 4-Medical treatment; 5-Pediatrics - Diagnosis; 6-Pediatrics - Non-medical treatment; 7-Pediatrics - Medical treatment; 8-Surgical treatment.

High Serum Adipocyte Fatty Acid Binding Protein Is Associated with Metabolic Syndrome in Patients with Type 2 Diabetes.

Adipocyte fatty acid binding protein (A-FABP) is a key mediator of obesity-related metabolic syndrome (MetS). The aim of this study was to evaluate the relationship between A-FABP concentration and MetS in type 2 diabetes mellitus (DM) patients. Fasting blood samples were obtained from 165 type 2 DM volunteers. MetS and its components were defined using diagnostic criteria from the International Diabetes Federation. Among 165 DM patients, 113 patients (68.5%) had MetS. Diabetic persons who had MetS had significantly higher A-FABP levels (P < 0.001) than those without MetS. Female DM persons had higher A-FABP level than man (P < 0.001). No statistically significant differences in A-FABP levels were found in use of statin, fibrate, or antidiabetic drugs. Multivariate forward stepwise linear regression analysis revealed that body fat mass (P < 0.001), logarithmically transformed creatinine (log-creatinine; P < 0.001), female DM patients (P < 0.001), and logarithmically transformed high sensitive C-reactive protein (log-hs-CRP; P = 0.013) were positively correlated, while albumin (P = 0.004) and glomerular filtration rate (GFR; P = 0.043) were negatively correlated with serum A-FABP levels in type 2 DM patients. In this study, higher serum A-FABP level was positively associated with MetS in type 2 DM patients.

Abstract 18950: Changes in Vasodilator Reactivity and Vasoconstrictor Tone in Metabolically Healthy Obesity and the Metabolic Syndrome

Background: Patients with obesity-related metabolic syndrome (MetS) have endothelial dysfunction due to decrease nitric oxide (NO) availability and increased endothelin (ET)-1-mediated vasoconstrictor tone. Given the prognostic significance of endothelial dysfunction, these abnormalities may be involved in the increased risk of cardiovascular mortality of these patients. Whether patients with metabolically healthy obesity (MHO), in whom those metabolic abnormalities that define the MetS are not present, have similar impairment of endothelial function is unknown. Methods: Forearm blood flow (FBF) responses were measured by strain-gauge plethysmography during intra-arterial infusion of graded-doses of acetylcholine (ACh; an endothelial-dependent vasodilator) and sodium nitroprusside (SNP; an endothelium-independent vasodilator), and/or during selective antagonism of ETA receptors by BQ-123 (10 nmol/min for 60 minutes) in lean subjects (n=56) and in obese patients (n=119), with either MHO (n=34) or the MetS (n=85). Results: ACh and SNP caused vasodilation in both obese and lean participants (all P&lt;0.001 vs. baseline). The response, however, to both agents was significantly lower in the obese than in the control group (both P&lt;0.001). Among the obese participants, the reactivity to ACh was higher in MHO than in the MetS (P&lt;0.001), whereas the responsiveness to SNP was equally impaired in both groups (P=0.45); this suggests higher degree of endothelial dysfunction in the MetS, but similar impairment of smooth muscle reactivity in MHO and the MetS. As expected, BQ-123 increased FBF in obese (P&lt;0001 vs. baseline), but not in lean participants, hence the FBF response to ETA receptor blockade was higher in both obese groups than in controls (both P&lt;0.001). In keeping with the ACh results, the FBF response to BQ-123 was significantly higher in patients with the MetS than in those with MHO (P=0.007). Conclusions: Patients with MHO have abnormal vascular reactivity, albeit their endothelial dysfunction is less pronounced than in patients with the MetS. These findings indicate that obesity per se is associated with some degree of vascular damage independently of those metabolic abnormalities underlying the MetS.

Endostatin Prevents Dietary-Induced Obesity by Inhibiting Adipogenesis and Angiogenesis.

Endostatin is a well-known angiogenesis inhibitor. Although angiogenesis has been considered as a potential therapeutic target of obesity, the inhibitory effect of endostatin on adipogenesis and dietary-induced obesity has never been demonstrated. Adipogenesis plays a critical role in controlling adipocyte cell number, body weight, and metabolic profile in a homeostatic state. Here we reveal that endostatin inhibits adipogenesis and dietary-induced obesity. The antiadipogenic mechanism of endostatin lies in its interaction with Sam68 RNA-binding protein in the nuclei of preadipocytes. This interaction competitively impairs the binding of Sam68 to intron 5 of mammalian target of rapamycin (mTOR), causing an error in mTOR transcript. This consequently decreases the expression of mTOR, results in decreased activities of the mTOR complex 1 pathway, and leads to defects in adipogenesis. Moreover, our findings demonstrate that the antiangiogenic function of endostatin also contributes to its obesity-inhibitory activity. Through the combined functions on adipogenesis and angiogenesis, endostatin prevents dietary-induced obesity and its related metabolic disorders, including insulin resistance, glucose intolerance, and hepatic steatosis. Thus, our findings reveal that endostatin has a potential application for antiobesity therapy and the prevention of obesity-related metabolic syndromes.

Aging, arterial stiffness, and hypertension.

Although the etiology of essential hypertension remains unknown, it is clear that multiple factors may contribute to the pathogenesis of hypertension. Hypertension is an outcome of the interaction of multiple genetic and environmental factors. Several epidemiological studies indicated that the incidence of arterial stiffness and hypertension and related cardiovascular disease (stroke, myocardial infarction) is higher in the aged than in the young population.1–4 The prevalence of arterial stiffening and hypertension increases with age.1,5 Based on an epidemiological study,6 the prevalence of hypertension is more than doubled in the elderly than in the young population. More than two-thirds of individuals after 65 years of age experience hypertension according to the Seventh Report of the Joint National Committee (JNC-7).7 Therefore, it is generally thought that hypertension is an aging disorder. In recent years, metabolic syndrome and hypertension are increasingly seen in the middle-aged and young populations. In these subpopulations, insulin resistance and overproduction of adipokines impair endothelial and heart function leading to early and accelerated cardiovascular aging. It was reported that premature aging (progeria) is associated with accelerated vascular stiffening or vascular aging.8 Aging is defined as the age-related decline in physiological function essential for survival and fertility. Cardiovascular aging is an important factor that determines life span. The wall of large conduit arteries, especially aorta, thicken and lose elasticity over time, and this process results in an increase in pulse wave velocity, an important and reliable measure of arterial stiffness. The increased arterial stiffness, whatever its underlying causes, would reduce the reservoir/buffering function of the conduit arteries near the heart and increase pulse wave velocity, both of which increase systolic and pulse pressure. Therefore, aging-related hypertension is characterized by a significant increase in systolic blood pressure with no change or even a …

Chlorogenic acid improves high fat diet-induced hepatic steatosis and insulin resistance in mice.

Chlorogenic acid (CGA), the most abundant component in coffee, has exhibited many biological activities. The objective of this study is to assess preventive and therapeutic effects of CGA on obesity and obesity-related liver steatosis and insulin resistance. Two sets of experiments were conducted. In set 1, 6-week old C57BL/6 mice were fed a regular chow or high-fat diet (HFD) for 15 weeks with twice intra-peritoneal (IP) injection of CGA (100 mg/kg) or DMSO (carrier solution) per week. In set 2, obese mice (average 50 g) were treated by CGA (100 mg/kg, IP, twice weekly) or DMSO for 6 weeks. Body weight, body composition and food intake were monitored. Blood glucose, insulin and lipid levels were measured at end of the study. Hepatic lipid accumulation and glucose homeostasis were evaluated. Additionally, genes involved in lipid metabolism and inflammation were analyzed by real time PCR. CGA significantly blocked the development of diet-induced obesity but did not affect body weight in obese mice. CGA treatment curbed HFD-induced hepatic steatosis and insulin resistance. Quantitative PCR analysis shows that CGA treatment suppressed hepatic expression of Pparγ, Cd36, Fabp4, and Mgat1 gene. CGA treatment also attenuated inflammation in the liver and white adipose tissue accompanied by a decrease in mRNA levels of macrophage marker genes including F4/80, Cd68, Cd11b, Cd11c, and Tnfα, Mcp-1 and Ccr2 encoding inflammatory proteins. Our study provides direct evidence in support of CGA as a potent compound in preventing diet-induced obesity and obesity-related metabolic syndrome. Our results suggest that drinking coffee is beneficial in maintaining metabolic homeostasis when on a high fat diet.

MicroRNAs Control Macrophage Formation and Activation: The Inflammatory Link between Obesity and Cardiovascular Diseases.

Activation and recruitment of resident macrophages in tissues in response to physiological stress are crucial regulatory processes in promoting the development of obesity-associated metabolic disorders and cardiovascular diseases. Recent studies have provided compelling evidence that microRNAs play important roles in modulating monocyte formation, macrophage maturation, infiltration into tissues and activation. Macrophage-dependent systemic physiological and tissue-specific responses also involve cell-cell interactions between macrophages and host tissue niche cell components, including other tissue-resident immune cell lineages, adipocytes, vascular smooth muscle and others. In this review, we highlight the roles of microRNAs in regulating the development and function of macrophages in the context of obesity, which could provide insights into the pathogenesis of obesity-related metabolic syndrome and cardiovascular diseases.

Hypertension and Obesity: Correlates With Renin‐Angiotensin‐Aldosterone System and Uric Acid

Arterial hypertension, obesity, the renin-angiotensinaldosterone system (RAAS), and uric acid are all independently ligated to an increased cardiovascular (CV) risk. Arterial hypertension and obesity are among the 20 leading risk factors that increase the mortality of the general population with hypertension, which is number one. In turn, obesity is one of the most common factors responsible for the development of arterial hypertension. On the other hand, the RAAS and uric acid have been shown to participate independently in the development and maintenance of arterial hypertension, as well as in the mechanisms leading to the development of hypertension in obesity. Furthermore, RAAS as well as uric acid have been shown to be related to an increase in CV morbidity and mortality in hypertension and obesity. In fact, uric acid could play a role in the epidemic of obesity-related metabolic syndrome and cardiorenal disease. In this issue of The Journal of Clinical Hypertension, Zhang and colleagues expand the knowledge of the participation of the RAAS and uric acid in the pathogenesis of hypertension in obesity. The authors describe that serum uric acid is strongly related to angiotensinogen in an obesity-dependent manner in untreated hypertensive patients. They also describe that serum uric acid seems to contribute to the enhancement of plasma angiotensinogen and could be involved in the pathophysiology of obesity-related hypertension where an increase in activity of RAAS is one of the mechanisms underlying the development and maintenance of arterial hypertension. The pathophysiological scene of hypertension in obesity is a vicious circle in which specific mechanisms can contribute at the same time to trigger others, leading to the progressive deterioration of the cardiorenal system. This crosstalk between hypertension and obesity is represented in the Figure where it is shown how these mechanisms are interconnected. In this context, hyperuricemia is strongly related to arterial hypertension. At the same time, increased sympathetic activity and increased RAAS are also mechanisms underlying hypertension and obesity, where the results of Zhang and colleagues also point to angiotensinogen as an important player in the pathogenesis of obesity hypertension. The high level of circulating angiotensinogen observed in untreated hypertensive obese patients is also likely

Metabolic disease risk in children by salivary biomarker analysis.

ObjectiveThe study of obesity-related metabolic syndrome or Type 2 diabetes (T2D) in children is particularly difficult because of fear of needles. We tested a non-invasive approach to study inflammatory parameters in an at-risk population of children to provide proof-of-principle for future investigations of vulnerable subjects.Design and MethodsWe evaluated metabolic differences in 744, 11-year old children selected from underweight, normal healthy weight, overweight and obese categories by analyzing fasting saliva samples for 20 biomarkers. Saliva supernatants were obtained following centrifugation and used for analyses.ResultsSalivary C-reactive protein (CRP) was 6 times higher, salivary insulin and leptin were 3 times higher, and adiponectin was 30% lower in obese children compared to healthy normal weight children (all P<0.0001). Categorical analysis suggested that there might be three types of obesity in children. Distinctly inflammatory characteristics appeared in 76% of obese children while in 13%, salivary insulin was high but not associated with inflammatory mediators. The remaining 11% of obese children had high insulin and reduced adiponectin. Forty percent of the non-obese children were found in groups which, based on biomarker characteristics, may be at risk for becoming obese.ConclusionsSignificantly altered levels of salivary biomarkers in obese children from a high-risk population, suggest the potential for developing non-invasive screening procedures to identify T2D-vulnerable individuals and a means to test preventative strategies.

Serum paraoxonase activity and oxidative stress and their relationship with obesity-related metabolic syndrome and non-alcoholic fatty liver disease in obese children and adolescents

Oxidative stress has been reported to be involved in the pathogenesis of metabolic disorders related with obesity. The aim of the study was to investigate the association of oxidative stress and paraoxonase activities with non-alcoholic fatty liver disease (NAFLD) as well as metabolic syndrome. A total of 109 obese children and adolescents and 44 healthy and lean control subjects were enrolled in the study. According to their ultrasonographic steatosis scores, they were classified into four groups as follows: healthy children; obese, non-NAFLD; obese, grade I-NAFLD; and obese, grade II-III NAFLD. The biochemical parameters and insulin resistance (HOMA-IR) were evaluated from fasting samples. The plasma total antioxidant status (TAS), total oxidant status (TOS), and serum paraoxonase activities were measured and then oxidative stress index (OSI) was calculated as the indicator of degree of oxidative stress. As the steatosis increased, the alanine aminotransferase, C-reactive protein, HOMA-IR, total cholesterol, and LDL cholesterol increased, whereas HDL cholesterol decreased. The TAS measurements were higher in the obese NAFLD group compared with that of the healthy control group. The TOS and OSI measurements did not differ between the groups. Paraoxonase activities increased significantly as steatosis increased. Among the children in this study, no relationship could be demonstrated between obesity with/without steatosis and oxidant/antioxidant status.

Relationship of High Sensitivity C-Reactive Protein Levels to Anthropometric and other Metabolic Parameters in Indian Children with Simple Overweight and Obesity.

High senstivity C-reactive protein (hsCRP) levels correlate well other parameters of obesity related metabolic syndrome (MS) and can be used as predictors of future cardiovascular disease risk. There is limited data on hsCRP levels in Indian children with simple obesity. To study the relationship of hsCRP levels with various anthropometric as well as metabolic parameters in children with simple overweight and obesity. This case control study was conducted in Paediatric Endocrinology clinic of a tertiary care hospital in Northern India. Levels of hsCRP were estimated in 100 overweight and obese children (BMI between 85(th) and 95(th) percentiles according to age & gender specific CDC 2000 growth charts) aged between 6 and 16 years and in 100 nearly age and sex matched healthy controls. These levels were then correlated to various anthropometric (body mass index, BMI; waist circumference, WC; hip circumference, HC; waist hip ratio, WHR; blood pressure) and biochemical (fasting blood glucose, FBG; total cholesterol, TC; high-density lipoprotein-cholesterol, HDL-C; low-density lipoprotein cholesterol, LDL-C; very low-density lipoprotein-cholesterol, VLDL-C; triglycerides, TG) parameters. Mean levels of hsCRP were significantly higher in the study group (3.92±2.20 versus 2.15±1.05 mg/L) as compared to controls. Significantly more (58% versus 10%) subjects in the study group had hsCRP (>3 mg/L). Of all the parameters studied, only BMI showed a positive correlation with hsCRP levels in the study group. Multiple logistic regression analysis for predicting outcome of high hsCRP showed positive correlation with BMI; with every 1 kg/m(2) increase in BMI, odds of high hsCRP level were increased by 37% (OR=1.37; 95% CI 1.23-1.53, p-value <0.0001). Mean values of all the biochemical parameters except HDL-C were significantly higher in the study group. Levels of hsCRP were significantly elevated in overweight and obese children as compared to non-obese children. In addition, these patients also showed abnormalities of lipid and glucose metabolism.

Curative diet supplementation with a melon superoxide dismutase reduces adipose tissue in obese hamsters by improving insulin sensitivity

Obesity-related metabolic syndrome is often associated with a decrease of insulin sensitivity, inducing several modifications. However, dietary antioxidants could prevent insulin resistance. We have previously shown the preventive effects of a melon superoxide dismutase (SOD) in obese hamsters. However, its antioxidant effects have never been studied on adipose tissue. We evaluated the effects of a 1-month curative supplementation with SODB on the adipose tissue of obese hamsters. Animals received either a standard diet or a cafeteria diet for 15 wk. Cafeteria diet induced obesity and related disorders, including insulin resistance and oxidative stress, in the abdominal adipose tissue. After SODB supplementation, the adipose tissue weight was decreased, probably by activating adipocytes lipolysis and thus reducing their size. SODB treatment also resulted in abdominal adipose tissue fibrosis reduction. Finally, SODB administration increased the expression of endogenous antioxidant enzymes and thus reduced oxidative stress and insulin resistance. The improvement of insulin sensitivity observed after SODB treatment could explain adipocyte lipolysis activation and fibrosis reduction. These findings demonstrate that a dietary SOD supplementation could be a useful strategy against obesity-related modifications in adipose tissue.

Obesity-related cardiorenal disease: the benefits of bariatric surgery

The inexorable increase in the prevalence of obesity is a global health concern, which will result in a concomitant escalation in health-care costs. Obesity-related metabolic syndrome affects approximately 25% of adults and is associated with cardiovascular and renal disease. The heart and kidneys are physiologically interdependent, and the pathological effects of obesity can lead to cardiorenal syndrome and, ultimately, kidney and heart failure. Weight loss can prevent or ameliorate obesity-related cardiorenal syndrome, but long-term maintenance of a healthy weight has been difficult to achieve through lifestyle changes or pharmacotherapy. Bariatric surgery offers both sustained weight loss and favourable metabolic changes, including dramatic improvements in glycaemic control and symptoms of type 2 diabetes mellitus. Procedures such as Roux-en-Y gastric bypass offer immediate multisystemic benefits, including bile flow alteration, reduced gastric size, anatomical gut rearrangement and altered flow of nutrients, vagal manipulation and enteric hormone modulation. In patients with cardiorenal syndrome, bariatric surgery also offers renoprotection and cardioprotection, and attenuates both kidney and heart failure by improving organ perfusion and reversing metabolic dysfunction. However, further research is required to understand how bariatric surgery acts on the cardiorenal axis, and its pioneering role in novel treatments and interventions for cardiorenal disease.

Prebiotics, faecal transplants and microbial network units to stimulate biodiversity of the human gut microbiome

SummaryAccumulating evidence demonstrates the intimate association between human hosts and the gut microbiome. Starting at birth, the sterile gut of the newborn acquires a diverse spectrum of microbes, needed for immunological priming. However, current practices (caesarean sections, use of formula milk) deprive newborns from being exposed to this broad spectrum of microbes. Unnecessary use of antibiotics and excessive hygienic precautions (e.g. natural versus chlorinated drinking water) together with the Western diet further contribute to a decreased microbial diversity in the adult gut. This has been correlated with recurrent Clostridium difficile infection, inflammatory bowel diseases and obesity, among others. A healthy gut microbiome is thus characterized by a diverse network of metabolically interacting microbial members. In this context, we review several existing and novel approaches to manage the gut microbiome. First, prebiotic compounds should be re-defined in the sense that they should enhance the ecological biodiversity rather than stimulating single species. Recent studies highlight that structurally different polysaccharides require specific primary degraders but also enhance a similar network of secondary degraders that benefit from cross-feeding. A faecal transplantation is a second approach to restore biodiversity when the microbiota is severely dysbiosed, with promising results regarding C. difficile-associated disease and obesity-related metabolic syndromes. A final strategy is the introduction of key microbial network units, i.e. pre-organized microbial associations, which strengthen the overall microbial network of the gut microbiome that supports human health.