Mass Obesity Research Articles

Ramadan Intermittent Fasting and Plasma Volume Variations in Individuals with Different Body Weights.

Background: There is increasing awareness of the physiological effects of Ramadan intermittent fasting (RIF) in obese subjects. However, there are no data on the effects of RIF on plasma volume changes (ΔPV) in individuals with different body weights. Background and Objectives: This study investigated the effects of RIF on ΔPV in normal-weight (NW) and overweight (OW) adult men, and adult men with obesity (OB) and severe obesity (SO). Materials and Methods: Thirty-two male subjects (32) were divided into four groups (n = 8 per group) according to their body mass index (BMI): normal weight (NW) (BMI < 25 kg/m2; age = 27.4 ± 3.8), overweight (OW) (BMI between 25 and 29.9 kg/m2; age = 26.8 ± 3.7), obese subjects (OB) (BMI between 30 and 34.9 kg/m2; age = 25.6 ± 2.9), and severely obesity (SO) (BMI between 35 and 40 kg/m2; age = 24.0 ± 4.1). Blood samples were collected for 24 h on 4 different occasions, at T0 before the start of the Ramadan month, at T1 15 days after the start of Ramadan, at T2 one day after the end of Ramadan, and at T3 on the 21st day after the end of Ramadan to determine ΔPV. All groups completed their fasting rituals for the 30 days of Ramadan. Results: A significant group × time effect occurred for body mass (p = 0.001; ES = 0.53), BMI (p = 0.001; ES = 0.53), and body fat percentage (p = 0.001; ES = 0.52). Post hoc tests indicated reductions in body mass in OB and SO at T1 (p = 0.03; ES = 0.21 and p = 0.002; ES = 0.12) and T2 (p = 0.03; ES = 0.31 and p = 0.02; ES = 0.23), reductions in BMI in OB and SO at T1 (p = 0.04; ES = 0.35 and p = 0.03; ES = 0.42) and T2 (p = 0.03; ES = 0.52 and p = 0.005; ES = 0.48), and reductions in body fat percentage only in OB AT T1 (p = 0.002; ES = 0.31) and T2 (p = 0.001; ES = 0.17). A significant group × time effect occurred for hematocrit (p = 0.02; ES = 0.34), hemoglobin (p = 0.01; ES = 0.35), and ΔPV (p = 0.02; ES = 0.18). Post hoc tests indicated increases in hematocrit in OB at T2 (p = 0.03; ES = 0.36) and hemoglobin in OB and SO at T1 (p = 0.03; ES = 0.35 and p = 0.002; ES = 0.32) and T2 (p = 0.003; ES = 0.21 and p = 0.002; ES = 0.33). There were also increases in ΔPV in OB at T1 and T2 (p = 0.002; ES = 0.25 and p = 0.003; ES = 0.22) and in SO only at T2 (p = 0.02; ES = 0.37). Contrast analysis indicated that NW was significantly lower than the grand mean of OW, Ob, and SO for all anthropometric and PVV variables (all p < 0.05). Conclusions: The effects of RIF on ΔPV and anthropometric characters was greater in obese individuals compared to normal-weight and overweight participants, suggesting that the improvements in body composition and ΔPV produced by RIF could positively influence obesity.

Study the Association of Fat Mass and Obesity-associated (FTO) Gene Polymorphisms (SNP rs9939609) with Biochemical Markers in Obese Iraqi Patients

This study aimed to evaluate the association of single nucleotide polymorphisms (SNP rs-9939609) of the fat mass and obesity-associated (FTO) gene with body mass index (BMI) and some biochemical markers in obese patients. The fat and mass obesity (FTO) gene variant specific single nucleotide polymorphism (SNP rs-9939609) with the T to A missense mutation may have a powerful association with obesity. This case-control study included 106 obese patients (57 males and 49 females) and 80 healthy control (40 males and 40 females). DNA was extracted from whole blood, and then the tetra-primer amplification refractory mutation system - polymerase chain reactions (ARMS.PCR) technique was used to limit the single nucleotide gene polymorphisms (rs9939609) of the FTO gene. Lipid profile, glycated hemoglobin (HbA1C), fasting blood sugar, insulin and FTO concentrations were measured by standard methods. In this study, the A allele in the rs9939609 was at a higher frequency of 35 (33.1%) in the obese patients and at a significant p-value = 0.039 compared with control 15 (18.7%). It significantly increased in the additive model and allele frequency (p= 0.003, 0.002 respectively). The rs9939608 SNP showed a significant association with increased BMI, insulin and homeostatic model assessment-insulin resistance (HOMO-IR) with p-values of 0.001, 0.001 and 0.028 respectively. After making adjustments for age and sex, lower levels of high-density lipoprotein (HDL) were observed in the AA and TA genotypes compared to the TT genotype (p = 0.004). While, no significant differences were recorded between the rs9939608 SNP and HbA1C, total cholesterol (TC), triglyceride (TG), very low-density lipoprotein (VLDL), and low-density lipoprotein (LDL) in obese patients

The Association of Serum Irisin with Impaired Glucose Before and After Laparoscopic Sleeve Gastrectomy in Obesity.

To demonstrate the association of irisin levels with impaired glucose before and after laparoscopic sleeve gastrectomy (LSG) in patients with obesity. Thirty-six patients with obesity undergoing LSG were included. We tested the irisin levels before and after LSG and conducted an evaluation of baseline irisin levels with elevated glucose as well as irisin changes with weight loss and its association with glucose control after LSG. Anthropometric measurements, body fat index, and metabolic parameters were significantly improved in 3months following LSG (all p < 0.05). Baseline irisin levels were significantly higher in obesity with elevated fasting glucose than that with normal glucose (2.98 [2.37, 3.63] vs. 3.72 [3.06, 5.32], p = 0.031). After adjustment for sex, gender, and body mass index (BMI), obesity with higher irisin levels was prone to have impaired fasting glucose (OR = 2.499, 95% CI = 1.047-5.964). According to receiver operating characteristic curve analysis, the diagnostic accuracy and sensitivity of baseline irisin levels on impaired fasting glucose were 75% and 77.8%. Irisin levels decreased from 3.29 (2.67, 4.43) to 2.82 (2.41, 3.25) ng/mL (p = 0.009) after LSG. The decreases of weight, BMI, and FFA were more in irisin changes group (△irisin ≥ 0.5) than in no irisin changes group (△irisin < 0.5). And △irisin was negatively associated with postprandial glucose (PG) at 3months after LSG (0.5h-PG, r = - 0.478, p = 0.029; 2h-PG, r = - 0.406, p = 0.017). Elevated baseline irisin levels indicated the impaired glucose in obesity. The decrease of irisin with weight loss provided more evidence for the contribution of serum irisin secretion by fat mass in obesity.

CD36 deficiency inhibits proliferation by cell cycle control in skeletal muscle cells.

Obesity-related muscular dysfunction and relative muscle atrophy affect an increasing number of people. Elucidating the molecular mechanisms of skeletal muscle cell development and growth may contribute to the maintenance of skeletal muscle mass in obesity. Fatty acid translocase (FAT/CD36), as a long-chain fatty acid transport protein, is crucial for lipid metabolism and signaling. CD36 is known to function in myogenic differentiation, and whether it affects the proliferation of skeletal muscle cells and the underlying mechanisms remain unclear. In this study, the effect of CD36 deficiency on skeletal muscle cell viability and proliferation was examined using C2C12 myoblasts. Results showed that the deletion of CD36 enhanced the inhibitory effect of PA on the proliferation and the promotion of apoptosis in skeletal muscle cells. Intriguingly, the silencing of CD36 suppressed cell proliferation by preventing the cell cycle from the G0/G1 phase to the S phase in a cyclin D1/CDK4-dependent manner. Overall, we demonstrated that CD36 was involved in skeletal muscle cell proliferation by cell cycle control, and these findings might facilitate the treatment of obesity-related muscle wasting.

Differences in mediterranean diet adherence on bmi, waist circumference, fat percentage, muscle mass in obesity

Obesity is a multifactorial disease that occurs when there is an abnormal accumulation of body fat due to an imbalance between energy intake and energy expenditure. The prevalence of Riset Kesehatan Dasar in 2018 showed that 21.8% of the Indonesian population over 18 years is obese. One of the diets recommended by European Association for the Study of Obesity Community for obesity is the Mediterranean diet. This study aims to determine the difference of adherence level in the Mediterranean diet to nutritional status, and muscle mass in obese patients. The method used in this study is analytic observational with prospective cohort observations. Subjects in this study were 37 obese patients who were monitored for diet four times in one month with food frequency questionnaire and checked for BMI, waist circumference, body fat percentage, and muscle mass at the end of the month. BMI and body fat percentage were analyzed using the Anova test while waist circumference and muscle mass data were analyzed using the Kruskal Wallis test. The level of adherence to the Mediterranean diet has been shown to significantly affect BMI (p=0.008), waist circumference (p=0.042), body fat percentage (p=0.014), and muscle mass (p=0.009) in obese patients. This associated with the composition of Mediterranean diet which affects increase in thermogenesis, fat oxidation, anti-inflammatory, and increases satiety for a longer period. The results of this study support the hypothesis that there is the difference of adherence to the Mediterranean diet to nutritional status and muscle mass in obese patients. DOI : 10.35990/amhs.v1n1.p28-37

Multipotent Stromal Cells from Subcutaneous Adipose Tissue of Normal Weight and Obese Subjects: Modulation of Their Adipogenic Differentiation by Adenosine A1 Receptor Ligands.

Adenosine A1 receptor (A1R) activation, stimulating lipogenesis and decreasing insulin resistance, could be useful for metabolic syndrome management in obese subjects. Since full A1R agonists induce harmful side-effects, while partial agonists show a better pharmacological profile, we investigated the influence of two derivatives of the full A1R agonist 2-chloro-N6-cyclopentyladenosine (CCPA), C1 and C2 behaving as A1R partial agonists in animal models, on the adipogenic differentiation of stromal/stem cells (ASCs) from human subcutaneous adipose tissue, which mainly contribute to increase fat mass in obesity. The ASCs from normal-weight subjects showed increased proliferation and A1R expression but reduced adipogenic differentiation compared to obese individual-derived ASCs. Cell exposure to CCPA, C1, C2 or DPCPX, an A1R antagonist, did not affect ASC proliferation, while mainly C2 and DPCPX significantly decreased adipogenic differentiation of both ASC types, reducing the activity of glycerol-3-phosphate dehydrogenase and the expression of PPARγ and FABP-4, all adipogenic markers, and phosphorylation of Akt in the phosphatidylinositol-3-kinase pathway, which plays a key-role in adipogenesis. While requiring confirmation in in vivo models, our results suggest that A1R partial agonists or antagonists, by limiting ASC differentiation into adipocytes and, thereby, fat mass expansion, could favor development/worsening of metabolic syndrome in obese subjects without a dietary control.

Polycystic ovary syndrome is linked with the fat mass obesity (FTO) gene variants rs17817449 and rs1421085 in western Saudi Arabia.

Polycystic ovary syndrome (PCOS) is characterised by infertility, obesity, insulin resistance and clinical and/or biochemical signs of hyperandrogenism. Obesity is known to be correlated with PCOS causing ovulatory dysfunction and hormone imbalances. Moreover, fat mass and the obesity gene (FTO) were linked with obesity and PCOS. Therefore, it is of interest to determine the genotype and allele frequency for three FTO variants - rs17817449 (G/T), rs1421085 (C/T) and rs8050136 (A/C) -in western Saudi population. 95 PCOS patients and 94 controls were recruited for this study. The genetic variants were assayed using real-time polymerase chain reaction using TaqMan genotyping assays. The chi-squared test was applied to investigate the difference between single nucleotide polymorphisms on PCOS and control subjects, and binary logistic regression was used to determine the association of FTO variants with PCOS symptoms. Variants rs17817449 and rs1421085 were significantly linked with PCOS susceptibility in the study population. Rs17817449 and rs8050136 were significantly associated with hair loss in the PCOS group. Furthermore, rs1421085 and rs8050136 were associated with a high body mass index (BMI>30 kg/m2). Risk alleles in our population associated with hair loss and elevated BMI in women with PCOS were homozygous C for rs8050136. This data will help in defining the genetic predisposition of PCOS among women in western Saudi Arabia.

Leptin in Atherosclerosis: Focus on Macrophages, Endothelial and Smooth Muscle Cells.

Increasing adipose tissue mass in obesity directly correlates with elevated circulating leptin levels. Leptin is an adipokine known to play a role in numerous biological processes including regulation of energy homeostasis, inflammation, vascular function and angiogenesis. While physiological concentrations of leptin may exhibit multiple beneficial effects, chronically elevated pathophysiological levels or hyperleptinemia, characteristic of obesity and diabetes, is a major risk factor for development of atherosclerosis. Hyperleptinemia results in a state of selective leptin resistance such that while beneficial metabolic effects of leptin are dampened, deleterious vascular effects of leptin are conserved attributing to vascular dysfunction. Leptin exerts potent proatherogenic effects on multiple vascular cell types including macrophages, endothelial cells and smooth muscle cells; these effects are mediated via an interaction of leptin with the long form of leptin receptor, abundantly expressed in atherosclerotic plaques. This review provides a summary of recent in vivo and in vitro studies that highlight a role of leptin in the pathogenesis of atherosclerotic complications associated with obesity and diabetes.

Full characterisation of knee extensors' function in ageing: effect of sex and obesity.

Muscle function is a marker of current and prospective health/independence throughout life. The effects of sex and obesity (OB) on the loss of muscle function in ageing remain unresolved, with important implications for the diagnosis/monitoring of sarcopenia. To characterise in vivo knee extensors' function, we compared muscles torque and power with isometric and isokinetic tests in older men (M) and women (W), with normal range (NW) of body mass index (BMI) and OB. In 70 sedentary older M and W (69 ± 5 years), NW and OB (i.e. BMI < 30 kg m-2 and ≥30 kg m-2, respectively) we tested the right knee's extensor: (i) isometric torque at 30°, 60°, 75° and 90° knee angles, and (ii) isokinetic concentric torque at 60, 90, 150, 180 and 210° s-1 angular speeds. Maximal isometric T-angle, maximal isokinetic knee-extensor torque-velocity, theoretical maximal shortening velocity, maximal power, optimal torque and velocity were determined in absolute units, normalised by body mass (BM) and right leg lean mass (LLMR) and compared over sex, BMI categories and angle or angular speeds by three-way ANOVA. In absolute units, relative to BM and LLMR, sex differences were found in favour of M for all parameters of muscle function (main effect for sex, p < 0.05). OB did not affect either absolute or relative to LLMR isometric and isokinetic muscle function (main effect for BMI, p > 0.05); however, muscle function indices, when adjusted for BM, were lower in both M and W with OB compared to NW counterparts (p < 0.05). We confirmed sex differences in absolute, relative to BM and LLMR muscle function in favour of men. While overall muscle function and muscle contractile quality is conserved in individuals with class I OB, muscle function normalised for BM, which defines the ability to perform independently and safely the activities of daily living, is impaired in comparison with physiological ageing.

Circulating exosome-like vesicles of humans with nondiabetic obesity impaired islet β-cell proliferation, which was associated with decreased Omentin-1 protein cargo

The regulation of β-cell mass in the status of nondiabetic obesity remains not well understood. We aimed to investigate the role of circulating exosome-like vesicles (ELVs) isolated from humans with simple obesity in the regulation of islet β-cell mass. Between June 2017 and July 2019, 81 subjects with simple obesity and 102 healthy volunteers with normal weight were recruited. ELVs were isolated by ultra-centrifugation. The proliferations of β-cells and islets were measured by 5-ethynl-2′-deoxyuridine (EdU). Protein components in ELVs were identified by Quantitative Proteomic Analysis and verified by Western blot and ELISA. The role of specific exosomal protein was analyzed by gain-of-function approach in ELVs released by 3T3-L1 preadipocytes. Circulating ELVs from subjects with simple obesity inhibited β-cell proliferation in vitro without affecting its apoptosis, secretion, and inflammation. The protein levels of Rictor and Omentin-1 were downregulated in circulating ELVs from subjects with simple obesity and associated with the obesity-linked pathologic conditions. The ELV-carried Omentin-1 and Omentin-1 protein per se were validated to increase β-cell proliferation and activate Akt signaling pathway. Moreover, Omentin-1 in ELVs was downregulated by insulin. The circulating ELVs may act as a negative regulator for β-cell mass in nondiabetic obesity through inhibiting β-cell proliferation. This effect was associated with downregulated Omentin-1 protein in ELVs. This newly identified ELV-carried protein could be a mediator linking insulin resistance to impaired β-cell proliferation and a new potential target for increasing β-cell mass in obesity and T2DM.

Beta-Cell Mass in Obesity and Type 2 Diabetes, and Its Relation to Pancreas Fat: A Mini-Review.

Type 2 diabetes (T2DM) is characterized by insulin resistance and beta-cell dysfunction. Although insulin resistance is assumed to be a main pathophysiological feature of the development of T2DM, recent studies have revealed that a deficit of functional beta-cell mass is an essential factor for the pathophysiology of T2DM. Pancreatic fat contents increase with obesity and are suggested to cause beta-cell dysfunction. Since the beta-cell dysfunction induced by obesity or progressive decline with disease duration results in a worsening glycemic control, and treatment failure, preserving beta-cell mass is an important treatment strategy for T2DM. In this mini-review, we summarize the current knowledge on beta-cell mass, beta-cell function, and pancreas fat in obesity and T2DM, and we discuss treatment strategies for T2DM in relation to beta-cell preservation.

The Cardiotonic Steroid Marinobufagenin Is a Predictor of Increased Left Ventricular Mass in Obesity: The African-PREDICT Study.

The endogenous Na+/K+-ATPase inhibitor, marinobufagenin (MBG), strongly associates with salt intake and a greater left ventricular mass index (LVMi) in humans and was shown to promote cardiac fibrosis and hypertrophy in animals. The adverse effects of MBG on cardiac remodeling may be exacerbated with obesity, due to an increased sensitivity of Na+/K+-ATPase to MBG. This study determined whether MBG is related to the change in LVMi over time in adults with a body mass index (BMI) ≥30 kg/m2 (obese) and <30 kg/m2 (non-obese). The study followed 275 healthy participants (aged 20–30 years) from the African-Prospective study on the Early Detection and Identification of Cardiovascular disease and Hypertension (African-PREDICT) study over 4.5 years. At baseline, we measured 24 h urine MBG excretion. MBG levels were positively associated with salt intake. LVMi was determined by two-dimensional echocardiography at baseline and after >4.5 years. With multivariate adjusted analyses in obese adults (N = 56), we found a positive association of follow-up LVMi (Adjusted (Adj.) R2 = 0.35; Std. β = 0.311; p = 0.007) and percentage change in LVMi (Adj. R2 = 0.40; Std. β = 0.336; p = 0.003) with baseline MBG excretion. No association of LVMi (Adj. R2 = 0.37; p = 0.85) or percentage change in LVMi (Adj. R2 = 0.19; p = 0.68) with MBG excretion was evident in normal weight adults (N = 123). These findings suggest that obese adults may be more sensitive to the adverse cardiac effects of MBG and provide new insight into the potential role of dietary salt, by way of MBG, in the pathogenesis of cardiac remodeling in obese individuals.

Evaluation of muscle mass in obesity, prediabetes and diabetes mellitus by different equations used for the measurement of muscle mass

ObjectiveInsulin resistance is one of risk factors for sarcopenia and there is no specific equation for the measurement of muscle mass. The present study aimed to evaluate muscle mass in the patients with obesity, prediabetes (PDM) and type 2 diabetes mellitus (DM) by different equations for the measurement of muscle mass. MethodsObese patients aged 18–65 years old, who presented between 2013 and 2015 were reviewed and they were separated into three groups as obese, prediabetes (PDM) and diabetes mellitus (DM). Height, body weight, body mass index (BMI), sum of the appendicular lean masses (ALM) were measured in all participants. Body muscle mass ratio was calculated as the total muscle mass divided by the body weight, and skeletal muscle index was calculated as the total muscle mass divided by the square of the height. In addition, ALM/weight, ALM/height2 and ALM/BMI ratios were also evaluated. ResultsA total of 1107 participants, of whom 666 (60.2%) were female, were enrolled into the study. Of the participants, 288 (%26.02) had obesity, 524 (%47.33) had PDM and 295 (26.65%) had DM. There was a significant difference in ALM/BMI ratio between the three groups for both genders (p = 0.003 for female and p = 0.003 for male). ALM/weight ratio and body muscle mass ratio were decreased between groups in female, whereas it was no difference in male (p = 0.003, p < 0.001 for females, respectively; p = 0.802, p = 0.840 for males, respectively). ConclusionsALM/BMI may be more accurate for the evaluation of muscle mass in middle-aged obese, PDM and DM subjects.

Limitations of Fat-Free Mass for the Assessment of Muscle Mass in Obesity

Background: A high amount of adipose tissue limits the accuracy of methods for body composition analysis in obesity. Objectives: The aim was to quantify and explain differences in fat-free mass (FFM) (as an index of skeletal muscle mass, SMM) measured with bioelectrical impedance analysis (BIA), dual energy X-ray absorptiometry (DXA), air displacement plethysmography (ADP), and deuterium dilution in comparison to multicompartment models, and to improve the results of BIA for obese subjects. Methods: In 175 healthy subjects (87 men and 88 women, BMI 20–43.3 kg/m², 18–65 years), FFM measured by these methods was compared with results from a 3- (3C) and a 4-compartment (4C) model. FFM_4C was compared with SMM measured by magnetic resonance imaging. Results: BIA and DXA overestimated and ADP underestimated FFM in comparison to 3C and 4C models with increasing BMI (all p < 0.001). ­Differences were largest for DXA. In obesity, BIA results were improved: value_corrected = ­value_uncorrected – a(BMI – 30 kg/m²), a = 0.256 for FFM and a = 0.298 for SMM. SMM accounts for 45% of FFM in women and 49% in men. Conclusions: In obesity, the use of FFM is limited by a systematic error of reference methods. In addition, SMM accounts for about 50% of FFM only. Corrected measurement of SMM by BIA can overcome these drawbacks.

Follow-up of a healthy lifestyle education program (the EdAl study): four years after cessation of randomized controlled trial intervention

BackgroundAn important challenge of school-based childhood obesity (OB) intervention programs is understanding the maintenance of the effects after cessation of the intervention to overcome the limitations of follow-up studies. The aim of this study is to verify the sustainability of the benefits achieved at a 4-year follow-up of the post-Educació en Alimentació (EDAl) program intervention cessation by assessing the OB-related outcomes and lifestyles of 13- to 15-year-old adolescents.MethodsThis paper describes a 4-year follow-up study after the cessation of a school-based randomized controlled intervention in adolescents (n = 349, intervention; n = 154, control) with baseline and 4-year follow-up data from high schools in Reus (intervention group), Salou, Cambrils and Vila-seca (control group). The outcomes are body mass index (BMI), BMI z-score, and OB prevalence according to the World Health Organization and International Obesity Task Force criteria and lifestyle data (obtained from questionnaires).ResultsCompared with the control girls, the intervention girls showed reduced BMI z-scores (−0.33 units, p < 0.01) from baseline (2007) to the 4-year follow-up post-intervention (2014). Compared with the control boys, the intervention boys showed reduced OB prevalence (−7.7%; p = 0.02). Compared with the control boys, more boys in the intervention group (19% increase; p = 0.059) showed ≥4 h/week after-school physical activity (PA). A decrease in the consumption of dairy products, fruits and fish was observed in both groups.ConclusionsAt the 4-year post-intervention follow-up of the EdAl program, compared with the control groups, girls had lower BMI z-scores and boys had lower OB prevalence from the intervention. The encouragement in after-school PA was long-lasting and maintained after the cessation of the intervention, whereas healthy food habits must be further reinforced in adolescents.Trial registrationISRCTN29247645.

The neuropeptide TLQP-21 opposes obesity via C3aR1-mediated enhancement of adrenergic-induced lipolysis

ObjectivesObesity is characterized by excessive fat mass and is associated with serious diseases such as type 2 diabetes. Targeting excess fat mass by sustained lipolysis has been a major challenge for anti-obesity therapies due to unwanted side effects. TLQP-21, a neuropeptide encoded by the pro-peptide VGF (non-acronymic), that binds the complement 3a receptor 1 (C3aR1) on the adipocyte membrane, is emerging as a novel modulator of adipocyte functions and a potential target for obesity-associated diseases. The molecular mechanism is still largely uncharacterized. MethodsWe used a combination of pharmacological and genetic gain and loss of function approaches. 3T3-L1 and mature murine adipocytes were used for in vitro experiments. Chronic in vivo experiments were conducted on diet-induced obese wild type, β1, β2, β3-adrenergic receptor (AR) deficient and C3aR1 knockout mice. Acute in vivo lipolysis experiments were conducted on Sprague Dawley rats. ResultsWe demonstrated that TLQP-21 does not possess lipolytic properties per se. Rather, it enhances β-AR activation-induced lipolysis by a mechanism requiring Ca2+ mobilization and ERK activation of Hormone Sensitive Lipase (HSL). TLQP-21 acutely potentiated isoproterenol-induced lipolysis in vivo. Finally, chronic peripheral TLQP-21 treatment decreases body weight and fat mass in diet induced obese mice by a mechanism involving β-adrenergic and C3a receptor activation without associated adverse metabolic effects. ConclusionsIn conclusion, our data identify an alternative pathway modulating lipolysis that could be targeted to diminish fat mass in obesity without the side effects typically observed when using potent pro-lipolytic molecules.

Reversible RNA Methylation In Gene Expression Regulation

We have discovered the first two RNA demethylases: FTO, a protein associated with human fat mass obesity and development, and ALKBH5, a protein that affects spermatogenesis in a mouse model. These two proteins catalyze oxidative demethylation of the most prevalent internal modifications of mammalian messenger RNA (mRNA) and other nuclear RNA, N6‐methyladenosine (m6A). These results indicate that reversible RNA modification could impact biological regulation analogous to the well‐known reversible DNA and histone chemical modifications. We have also identified and characterized proteins that can selectively recognize m6A‐modified mRNA and affect the translation status and lifetime of the target mRNA, as well as molecular machines that deposit the m6A methylation on nuclear RNA. Our discoveries indicate the presence of a new mode of biological regulation that depends on reversible and dynamic RNA modifications.

Sarcopenic obesity

“Sarcopenic obesity” describes the confluence of low muscle mass and/or strength with obesity in older adults, thought to contribute to increased risk for poor health outcomes compared to either condition alone. Despite almost 20 years of research into sarcopenic obesity, it currently lacks a consensus definition and this is a barrier to research and clinical investigations. This narrative review summarises current evidence of the role of sarcopenic obesity in age-related declines in musculoskeletal and cardiometabolic health, and potential treatment strategies. Research to date suggests that sarcopenic obesity, when defined by low muscle strength, contributes to significantly increased risk for poor physical function and possibly falls. It is likely that sarcopenic obese individuals have reduced bone quality relative to obese alone, and combined with an increased falls risk, may be predisposed to increased risk for fractures. Low muscle mass in obesity may also be associated with increased risk for cardiovascular disease, type II diabetes and mortality, however prospective studies are required to confirm the effects of sarcopenic obesity on musculoskeletal and cardiometabolic health in older adult populations. Similarly, large-scale randomised controlled trials are needed to clarify the most effective methods for reducing prevalence and incidence of sarcopenic obesity, but it is likely that lifestyle modification interventions which combine aerobic and resistance training, caloric restriction, and protein and/or vitamin D supplementation, may be most effective.

Molecular ecological tools to decipher the role of our microbial mass in obesity.

After birth, our gastrointestinal (GI) tract is colonised by a highly complex assemblage of microbes, collectively termed the GI microbiota, that develops intimate interactions with our body. Recent evidence indicates that the GI microbiota and its products may contribute to the development of obesity and related diseases. This, coupled with the current worldwide epidemic of obesity, has moved microbiome research into the spotlight of attention. Although the main cause of obesity and its associated metabolic complications is excess caloric intake compared with expenditure, differences in GI tract microbial ecology between individuals might be an important biomarker, mediator or new therapeutic target. This can be investigated using a diverse set of complementary so called -omics technologies, such as 16S ribosomal RNA gene-targeted composition profiling, metabolomics, metagenomics, metatranscriptomics and metaproteomics. This review aims to describe the different molecular approaches and their contributions to our understanding of the role of the GI microbiota in host energy homeostasis. Correspondingly, we highlight their respective strengths, but also try to create awareness for their specific limitations. However, it is currently still unclear which bacterial groups play a role in the development of obesity in humans. This might partly be explained by the heterogeneity in genotype, lifestyle, diet and the complex ethology of obesity and its associated metabolic disorders (OAMD). Nevertheless, recent research on this matter has shown a conceptual shift by focusing on more homogenous subpopulations, through the use of both anthropometric (weight, total body fat) as well as biochemical variables (insulin resistance, hyperlipidaemia) to define categories. Combined with technological advances, recent data suggests that an OAMD associated microbiota can be characterised by a potential pro-inflammatory composition, with less potential for the production of short chain fatty acids and butyrate in particular.

Vitamin D status is a determinant of skeletal muscle mass in obesity according to body fat percentage

ObjectivesVitamin D deficiency is now being recognized as an emerging problem worldwide. Obesity has been found to be associated with lower serum 25-hydroxyvitamin D [25(OH)D] concentrations due to various mechanisms. There is increasing evidence showing the extraskeletal health benefit of vitamin D. Previous studies demonstrated the relationship between vitamin D and adiposity. However, the association between vitamin D status and skeletal muscle mass has not been established in healthy obese individuals in tropical countries. The aim of this cross-sectional study was to assess vitamin D status and its relationship to serum 25(OH)D concentrations and body composition, including skeletal muscle mass (SMM) and adiposity in healthy obese individuals without diabetes who live in Thailand, which is located near the equator. MethodsWe enrolled 163 obese Thai individuals (59.5% women) from the obesity clinic at the Ramathibodi Hospital, Mahidol University, in Bangkok, Thailand. ResultsThe prevalence of vitamin D deficiency (<20 ng/mL) and vitamin D inadequacy (<30 ng/mL) were 49 (30.1%) and 148 (90.8%), respectively. In all, 98% of the individuals with body mass index >35 kg/m2 had vitamin D inadequacy. Serum 25(OH)D concentrations were negatively associated with percent body fat (%BF) (r = −0.23; P = 0.003). Moreover, vitamin D status was positively associated with SMM (r = 0.18; P = 0.03) and the association remained after controlling for body fat mass and age (P = 0.003). Interestingly, in the individuals with lowest tertile of %BF, multiple linear regression analysis revealed that the significant positive predictors of %SMM were vitamin D status and male sex; the negative predictor was the body mass index after adjusting for age and exercise duration. ConclusionsOur study demonstrated the high prevalence of vitamin D deficiency in obese, Thai populations without diabetes. Vitamin D status was an independent predictor of %SMM of patients with lowest tertile of %BF. We speculated that adiposity might play a role in the relationship of vitamin D and SMM.