Reduced Body Adiposity Research Articles

Lean metabolic dysfunction-associated steatotic disease is reversed by betulinic acid, a therapeutic triterpene from birch bark

The prevalence of metabolic dysfunction-associated steatotic disease (MASLD) in lean individuals has continued to increase. Despite the benefits of betulinic acid in obesity, its role in lean MASLD has not been verified. We investigated whether betulinic acid recovered lean MASLD by rescuing lipid homeostasis in vivo. Lean MASLD disease mice model was established using atherogenic diets on C57BL/6 male mice. Betulinic acid (5, 15, and 25 mg/kg bw) or positive control was provided ad libitum for 12 weeks. Betulinic acid reduced body adiposity (p < 0.01) without affecting lean mass. Betulinic acid improved hepatic lipid accumulation (p < 0.01). Blood lipid profiles, including triglyceride, total cholesterol, LDL-cholesterol, and non-esterified fatty acids (p < 0.001 and p < 0.05), were decreased by betulinic acid. RNA transcriptomes and immunoblotting revealed that betulinic acid markedly reduced hepatic de novo lipogenesis by inhibiting Srebp1/Acc/Fas (p < 0.05). Betulinic acid increased fatty acid utilization (p < 0.05) in skeletal muscle by stimulating Ampk/Acc1/Cpt1. These findings imply that betulinic acid is a potent bioactive compound that prevents lean MASLD and dyslipidemia.

SCD4 deficiency decreases cardiac steatosis and prevents cardiac remodeling in mice fed a high-fat diet

Stearoyl-CoA desaturase (SCD) is a lipogenic enzyme that catalyzes formation of the first double bond in the carbon chain of saturated fatty acids. Four isoforms of SCD have been identified in mice, the most poorly characterized of which is SCD4, which is cardiac-specific. In the present study, we investigated the role of SCD4 in systemic and cardiac metabolism. We used WT and global SCD4 KO mice that were fed standard laboratory chow or a high-fat diet (HFD). SCD4 deficiency reduced body adiposity and decreased hyperinsulinemia and hypercholesterolemia in HFD-fed mice. The loss of SCD4 preserved heart morphology in the HFD condition. Lipid accumulation decreased in the myocardium in SCD4-deficient mice and in HL-1 cardiomyocytes with knocked out Scd4 expression. This was associated with an increase in the rate of lipolysis and, more specifically, adipose triglyceride lipase (ATGL) activity. Possible mechanisms of ATGL activation by SCD4 deficiency include lower protein levels of the ATGL inhibitor G0/G1 switch protein 2 and greater activation by protein kinase A under lipid overload conditions. Moreover, we observed higher intracellular Ca2+ levels in HL-1 cells with silenced Scd4 expression. This may explain the activation of protein kinase A in response to higher Ca2+ levels. Additionally, the loss of SCD4 inhibited mitochondrial enlargement, NADH overactivation, and reactive oxygen species overproduction in the heart in HFD-fed mice. In conclusion, SCD4 deficiency activated lipolysis, resulting in a reduction of cardiac steatosis, prevented the induction of left ventricular hypertrophy, and reduced reactive oxygen species levels in the heart in HFD-fed mice.

Interleukin-6: An Under-Appreciated Inducer of Thermogenic Adipocyte Differentiation.

Adipose tissue inflammation is a key factor leading to obesity-associated immune disorders, such as insulin resistance, beta cell loss in the pancreatic islets, meta-inflammation, and autoimmunity. Inhibiting adipose tissue inflammation is considered a straightforward approach to abrogate these diseases. However, recent findings show that certain pro-inflammatory cytokines are essential for the proper differentiation and functioning of adipocytes. Lipolysis is stimulated, and the thermogenic competence of adipocytes is unlocked by interleukin-6 (IL-6), a cytokine that was initially recognized as a key trigger of adipose tissue inflammation. Coherently, signal transducer and activator of transcription 3 (STAT3), which is a signal transducer for IL-6, is necessary for thermogenic adipocyte development. Given the impact of thermogenic adipocytes in increasing energy expenditure and reducing body adiposity, functions of IL-6 in the adipose tissue have gained attention recently. In this review, we show that IL-6 signaling may protect from excess fat accumulation by stimulating thermogenesis in adipocytes.

Monounsaturated fat-rich diet reduces body adiposity in women with obesity, but does not influence energy expenditure and substrate oxidation: a parallel randomized controlled clinical trial.

Obesity is an important and growing health problem whose treatment involves dietary changes. In this context, studying the role of macronutrients in weight loss is required in order to understand which strategies may be applied for weight loss. We aimed to evaluate the effects of diets rich in polyunsaturated (PUFAs) and monounsaturated fatty acids (MUFAs) on resting energy expenditure (REE), substrate oxidation, and weight loss in women with obesity. Randomized, controlled, single blind, parallel-group clinical trial was conducted for 60 days. Participants (n = 32) were divided into three groups: G1= normocaloric PUFAs-rich diet (12% of total energy expenditure (TEE), 10% of n-6 and up to 2% of n-3); G2= normocaloric MUFAs-rich diet (15-20% TEE); and G3= maintenance of the usual diet. Anthropometric and metabolic variables (REE and substrate oxidation by indirect calorimetry) were evaluated. G2 decreased body weight (-1.92 ± 1.99 kg, P = 0.02), body mass index (BMI) (-0.69 ± 0.70 kg/m2; P = 0.02), waist circumference (WC) (-1.91 ± 1.82 cm; P = 0.02), and body fat (-1.14 ± 1.53 kg; P = 0.04). MUFAs-rich diet reduces body weight, BMI, body fat, and WC. NCT02656940. Clinical Trials: NCT02656940.

Association of Hibiscus sabdariffa and high-intensity interval training induces reduction in adiposity and beneficial metabolic adaptations in obesity without changes in lipid metabolism.

High-intensity interval training (HIIT) has stood out as a treatment for obesity, leading to adaptations of the cardiovascular system and reducing body adiposity. In addition, the search for alternative therapies for weight loss has intensified. The administration of Hibiscus sabdariffa (Hs) has been described as an efficient supplement in weight loss and in the treatment of metabolic changes associated with obesity. In this context, the objective was to investigate the effects of the association of Hs and HIIT on metabolic adaptations and lipid metabolism in obese rats. Wistars rats were subjected to obesity and subsequently randomized into 4 groups: obese (Ob), obese + HS (ObHs), obese + HIIT (ObHIIT), and obese + HS + HIIT (ObHsHIIT). For 8 weeks, ObHs and ObHsHIIT rats received Hs extract daily (150 mg/kg of body weight) and trained groups (ObHIIT and ObHsHIIT) were subjected to a HIIT program on a treadmill. Nutritional profile, glycemic curve, biochemical profile, and liver glycogen were determined. HIIT decreased caloric intake, feed efficiency, body adiposity, total body fat, and body weight gain, associated with improvements in physical performance parameters and a smaller glycemic curve and area. Hs had a hepatoprotective effect, reducing alkaline phosphatase values, but its effects were more pronounced when associated with HIIT. Therefore, the combination of treatments promoted a reduction in food consumption and body adiposity, as well as an improvement in physical performance and glycemic profile, but without changes in lipid metabolism.

Lower Adherence to a Mediterranean Diet Is Associated with High Adiposity in Community-Dwelling Older Adults: Results from the Longevity Check-Up (Lookup) 7+ Project

High adiposity impacts health and quality of life in old age, owing to its association with multimorbidity, decreased physical performance, and frailty. Whether a high adherence to a Mediterranean diet (Medi-Diet) is associated with reduced body adiposity in older adults is unclear. The present study was conducted to assess the prevalence of high adiposity in a large sample of community-dwelling older adults. We also explored the relationship between whole-body adiposity estimated through relative fat mass (RFM) and Medi-Diet adherence. Data were obtained from the Longevity Check-up 7+ (Lookup7+) project database. RFM was estimated from anthropometric and personal parameters using a validated equation. RFM was categorized as high if ≥40% in women and ≥30% in men. Information on diet was collected using a food frequency questionnaire, while Medi-Diet adherence was assessed through a modified version of the Medi-Lite scoring system. Analyses were conducted in 2092 participants (mean age 73.1 ± 5.9 years; 53.4% women). Mean RFM was 39.6 ± 5.14% in women and 29.0 ± 3.6% in men. High adiposity was found in 971 (46.4%) participants and was more frequent in those with a low (54.2%) or moderate (46.4%) Medi-Diet adherence compared with the high-adherence group (39.7%, p &lt; 0.001). Logistic regression indicated that older adults with high Medi-Diet adherence were less likely to have a high RFM. Other factors associated with a greater risk of having high adiposity were older age, female sex, and physical inactivity. Our findings support an association between healthy lifestyles, including a greater adherence to a Mediterranean-style diet, and lower body adiposity in older adults.

Bile salt dietary supplementation promotes growth and reduces body adiposity in gilthead seabream (Sparus aurata)

Bile salt dietary supplementation promotes growth and reduces body adiposity in gilthead seabream (Sparus aurata)

Black and Yellow Soybean Consumption Prevents High-Fat Diet-Induced Obesity by Regulating Lipid Metabolism in C57BL/6 Mice.

To evaluate the antiobesity effects of yellow and black soybean, C57BL/6 mice were provided with a normal diet, high-fat diet, HFD-containing yellow soybean powder (YS), and black soybean powder (BS) for six weeks. Compared with the HFD group, both YS and BS decreased body weight by 30.1% and 37.2% and fat in tissue by 33.3% and 55.8%, respectively. Simultaneously, both soybeans significantly reduced the serum triglyceride and total cholesterol levels and regulated the lipogenic mRNA expressions of Pparγ, Acc, and Fas genes in the liver, supporting reduced body adiposity. Furthermore, BS significantly increased Pgc-1α and Ucp1 mRNA expression levels in epididymal adipose tissue, indicating thermogenesis is the key mechanism of BS. Taken together, our findings suggest that both soybeans prevent high-fat diet-induced obesity in mice by regulating lipid metabolism, and BS, in particular, has a greater antiobesity potential than YS.

The Effectiveness of GLP-1 Receptor Agonist Semaglutide on Body Composition in Elderly Obese Diabetic Patients: A Pilot Study

Background and Objectives: This study aimed to investigate the changes in obesity severity, glucose metabolism, and body composition in patients with obesity and type 2 diabetes mellitus treated with glucagon-like peptide 1 receptor agonist (GLP1-RA) semaglutide. Materials and Methods: Body weight (BW), metabolic parameters, and body composition were examined before and 3 months after semaglutide administration. The mass of body fat (FM), fat weight percentage (%FM), mass of skeletal muscle (MM), skeletal MM percentage (%MM), and limb muscles were measured using the bioelectrical impedance method. Results: Semaglutide dramatically reduced the weight, the body mass index (BMI), and the levels of the glucose metabolic markers, including fasting blood glucose and hemoglobin A1c, and accelerated the loss of excess BW. FM, MM, and %FM after semaglutide treatment also decreased. Conversely, semaglutide had no effect on the %MM after 3 months. In limb muscle analyses, right upper and lower leg muscle percentages, left upper and lower leg muscles, and the ratios of the lower/upper muscles were maintained by semaglutide treatment. Conclusions: These results suggest that the GLP1-RA semaglutide effectively reduces body adiposity while maintaining the MM in obese type 2 diabetic patients.

Increasing energy expenditure through exercise and low ambient temperature offers oxidative protection to the hypothalamus after high-fat feeding to mice.

The effects of weight loss produced by increased energy expenditure on measures of oxidative stress and mitochondrial damage have not been investigated in the hypothalamus of diet-induced obese mice. The present study aimed to characterize the effects of either a low housing temperature of 17°C or daily exercise on a treadmill on high-fat diet (HFD)-induced abnormalities in the hypothalamic tissue of mice. Exercise and low ambient temperature protocols were designed to produce energy deficit through increased energy expenditure. Forty mice aged 8weeks were assigned to one of four conditions: chow diet (n=10), HFD (n=10), HFD and 5weeks of either exercise training (ET; n=10) or an ambient temperature of 17°C (n=10). Mice were killed at the age of 31weeks. In comparison with HFD treatment alone, both interventions reduced body adiposity (14.6% and 27.6% reduction for the ET and 17°C groups, respectively). Moreover, exposing obese mice to ET and 17°C restored mitochondrial DNA content (41.3% and 32.6% increase for the ET and 17°C groups, respectively), decreased level of lipid peroxidation as assessed by the detection of 4-hydroxy-nonenal protein adducts (12.8% and 29.4% reduction for the ET and 17°C groups, respectively) and normalized the expression levels of proinflammatory cytokines (Tnfα: 73.9% and 62%; Il1β: 54.5% and 39.6%; Il6: 33.1% and 35.6% reduction for the ET and 17°C groups, respectively), as well as several proteins associated with mitochondrial respiratory chain (OxPhos Complex I: 75.7% and 53.9%; Complex III: 33% and 36%; Complex V: 42% and 36.9% reduction for the ET and 17°C groups, respectively) in hypothalamic cells. Negative energy balance induced through either lower ambient temperature or exercise resulted in substantial and similar improvements in markers of inflammation and mitochondrial damage in the hypothalamus of mice with diet-induced obesity, potentially by reducing oxidative stress.

Dietary excess regulates absorption and surface of gut epithelium through intestinal PPAR\u03b1

Intestinal surface changes in size and function, but what propels these alterations and what are their metabolic consequences is unknown. Here we report that the food amount is a positive determinant of the gut surface area contributing to an increased absorptive function, reversible by reducing daily food. While several upregulated intestinal energetic pathways are dispensable, the intestinal PPARα is instead necessary for the genetic and environment overeating–induced increase of the gut absorptive capacity. In presence of dietary lipids, intestinal PPARα knock-out or its pharmacological antagonism suppress intestinal crypt expansion and shorten villi in mice and in human intestinal biopsies, diminishing the postprandial triglyceride transport and nutrient uptake. Intestinal PPARα ablation limits systemic lipid absorption and restricts lipid droplet expansion and PLIN2 levels, critical for droplet formation. This improves the lipid metabolism, and reduces body adiposity and liver steatosis, suggesting an alternative target for treating obesity.

Short-term combined training reduces hepatic steatosis and improves hepatic insulin signaling

Hepatic steatosis is directly associated with hepatic inflammation and insulin resistance, which is correlated with hyperglycemia and type 2 diabetes mellitus (T2DM). Aerobic and strength training have been pointed out as efficient strategies against hepatic steatosis. However, little is known about the effects of the combination of those two protocols on hepatic steatosis. Therefore, this study aimed to evaluate the impact of short-term combined training (STCT) on glucose homeostasis and in the synthesis and oxidation of fat in the liver of obesity-induced mice with hepatic steatosis. Swiss mice were distributed into three groups: control lean (CTL), sedentary obese (OB), and combined training obese (CTO). The CTO group performed the STCT protocol, which consisted of strength and aerobic exercises in the same session. The protocol lasted seven days. The CTO group reduced the glucose levels and fatty liver when compared to the OB group. Interestingly, these results were observed even without reductions in body adiposity. CTO group also showed increased hepatic insulin sensitivity, with lower hepatic glucose production (HGP). STCT reduced the expression of the lipogenic genes Fasn and Scd1 and hepatic inflammation, as well as increased the ACC phosphorylation and the oxidative genes Cpt1a and Ppara, reverting the complications caused by obesity. Since this protocol increased lipid oxidation and reduced hepatic lipogenesis, regardless of body fat mass decrease, it can be considered an effective non-pharmacological strategy for the treatment of hepatic steatosis.

Voluntary running of defined distances alters bone microstructure in C57BL/6 mice fed a high-fat diet.

Obesity increases the risk for pathological conditions such as bone loss. On the other hand, physical exercise reduces body adiposity. To test the hypothesis that physical activity improves bone quality, we evaluated voluntary running of defined distances on trabecular and cortical microstructure in mice fed a high-fat diet (HFD). Sedentary mice were fed the standard AIN93G diet or the HFD. Mice fed the HFD remained sedentary or were assigned to unrestricted running or 75%, 50%, and 25% of unrestricted running with an average running activity at 8.3, 6.3, 4.2, and 2.1km per day, respectively. The bone structural differences found in sedentary mice were that HFD, compared with the AIN93G diet, resulted in a lower bone volume fraction (BV/TV) and a higher structure model index (SMI) in vertebrae. Running had a greater effect on trabecular microstructure in femurs than in vertebrae; the decrease in SMI and an increase in trabecular thickness (Tb.Th) were in dose-dependent manners. Running was positively correlated with BV/TV and Tb.Th and inversely correlated with SMI in femurs. The HFD increased plasma concentrations of tartrate-resistant acid phosphatase 5b, a marker of bone resorption, in sedentary mice, while running decreased it in a dose-dependent manner. The findings show that voluntary running improves bone quality in young adult mice fed an HFD. Novelty: The high-fat diet alters bone microstructure by increasing bone resorption. Quantitative voluntary running improves bone microstructure through its attenuation of bone resorption in mice fed a high-fat diet.

1099-P: Effects of Empagliflozin on Glucose Metabolism and Body Fat Composition in Patients with Prediabetes: A Randomized, Double-Blind, Placebo-Controlled Trial

Objective: In patients with diabetes, the beneficial effects of empagliflozin on glucose metabolism, body adiposity, and liver fat content are well established. As the mode of action of SGLT2 inhibitors partly depends on elevated blood glucose, we investigated if these effects also occur in prediabetes. Methods: Forty participants with prediabetes (mean ± SD: age: 60 ± 9 years; BMI: 31.5 ± 3.8 kg/m²; FG: 5.98 ± 0.57 mmol/l) were randomized to receive 25 mg empagliflozin qd or placebo for 8 weeks. Before and after treatment, all participants underwent a 75 g oral glucose tolerance test to evaluate glucose tolerance, peripheral insulin sensitivity and insulin secretion. Body fat was assessed by whole-body MRI and intrahepatic fat by localized MR-spectroscopy. Resting energy expenditure and respiratory quotient (RQ) were assessed by indirect calorimetry at fast. “Per protocol” analysis using ANCOVA was performed. Results: Fasting glucose, glucose tolerance, peripheral insulin sensitivity, and insulin secretion were not significantly changed by treatment. Though, after 8 weeks of treatment, total adipose tissue (mean difference between groups at the end of study ± SEM: 3.1 ± 2.3 liters; p=0.034) and intrahepatic fat (2.1 ± 2.3 %; p=0.029) were lower in patients who received empagliflozin, compared to placebo. Empagliflozin treatment resulted in a lower RQ compared to placebo (p=0.022) without differences in resting energy expenditure (p=0.2), indicating preferential lipid oxidation upon treatment. Conclusion: In prediabetes, treatment with empagliflozin for 8 weeks has no major effects on glucose metabolism. However, this SGLT2 inhibitor reduced body adiposity and liver fat content, presumably by shifting energy metabolism towards lipid oxidation. Therefore, empagliflozin might represent a treatment option for obesity and hepatic steatosis in prediabetes, independent of drug effects on blood glucose. Disclosure J. Hummel: None. C. Dannecker: None. L. Fritsche: None. A. Vosseler: None. K. Kantartzis: None. S. Kullmann: None. J. Machann: None. H. Preissl: None. H. Haering: None. A. Fritsche: None. R. Wagner: Advisory Panel; Self; Novo Nordisk A/S. Speaker’s Bureau; Self; Novo Nordisk A/S. Other Relationship; Self; Eli Lilly and Company. M. Heni: Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc., Sanofi. Speaker’s Bureau; Self; Novo Nordisk A/S. Funding Boehringer Ingelheim

Chronic hindbrain administration of oxytocin elicits weight loss in high fat diet‐induced obese mice

Previous studies indicate that oxytocin (OXT) reduces body weight (BW) in high fat diet (HFD)‐induced obese (DIO) rodents through mechanisms that may involve an enhanced ability of OXT to reduce food intake as well as increase energy expenditure. We have previously demonstrated that chronic fourth ventricular (4V) infusions of OXT (as a strategy to target hindbrain OXT receptors) evokes weight loss in DIO rats. Based on these findings, we hypothesized that increased hindbrain OXT signaling would elicit BW loss in DIO mice maintained on a HFD (60% kcal from fat). To test this hypothesis, age‐matched mice were fed HFD or chow for 4 months prior to implantation of 4V cannulas and 28‐day minipumps that infused OXT (16 nmol/day) or vehicle (VEH; saline). Food intake and BW were tracked for 28 days. Body composition was assessed immediately prior to VEH or OXT treatment and near treatment completion using Quantitative Magnetic Resonance (QMR; EchoMRI 4‐in‐1). OXT preferentially reduced BW by approximately 4.5±1.4% in DIO mice relative to chow‐fed mice (P&lt;0.05; N=9–11/group). OXT‐elicited BW loss was associated with reductions in body adiposity, adipocyte size [inguinal white adipose tissue (IWAT)] and serum leptin (P&lt;0.05). These effects were attributed, in part, to an enhanced effect of OXT to reduce energy intake in DIO mice (P&lt;0.05) at a dose that was not associated with increased kaolin intake (pica behavior; P=NS). While reductions in energy intake contribute to OXT’s effects on BW, chronic 4V OXT appeared to increase uncoupling protein‐1 (UCP‐1) expression in IWAT (0.05&lt;P&lt;0.1; N=9–10/group) suggesting that OXT may also stimulate beiging of WAT. To assess OXT‐elicited changes in brown adipose tissue (BAT) thermogenesis, we examined the effects of acute 4V injections of OXT on interscapular BAT temperature (TIBAT) in mice. Consistent with our previous findings in rats, preliminary data in mice indicate that acute 4V injections of a lower dose (1 μg) appeared to elevate TIBAT at 0.5‐ (P=0.1) and 1.25‐h post‐injection (P=0.15) while a higher dose (5 μg) appeared to elevate TIBAT at 1.5‐ (P&lt;0.05) and 4‐h (0.05&lt;P&lt;0.1) post‐injection (N=4/group). Together, these findings support the hypothesis that chronic hindbrain OXT treatment evokes sustained weight loss in DIO mice by reducing energy intake and increasing BAT thermogenesis and beiging of WAT at a dose that is not associated with visceral illness.Support or Funding InformationNational Institutes of Health R01 DK115976 and VA Merit Review Award BX004102

Abstract 1608: Time-restricted feeding attenuates pulmonary metastasis of Lewis lung carcinoma in mice fed a high-fat diet

Abstract Circadian rhythms, which cycle approximately every 24 hours, control patterns of daily functions, e.g. feeding and fasting, rest and activity, and sleeping and waking. Altering the finely tuned circadian rhythms by an erratic lifestyle (e.g. disruption of the daily feeding and fasting pattern) leads to metabolic disorders, including obesity. Obesity is a risk factor for cancer. Obese cancer patients are at a greater risk of recurrence and metastasis than patients with normal body weight. We hypothesized that time-restricted feeding (TRF) attenuates high-fat diet-enhanced metastasis. In a metastasis model of Lewis lung carcinoma (LLC), male C57BL/6 mice were fed the standard AIN93G diet (16% of energy from soybean oil) or a high-fat diet (HFD) containing 45% of energy from soybean oil with or without dark phase restricted feeding (12 hours per day) for 10 weeks. Pulmonary metastases from a primary tumor, established by subcutaneous injection of LLC cells, were quantified. The percent fat body mass of the TRF group was lower than that of the HFD group and remained similar to that of the AIN93G group. There was no difference in energy intake between the TRF and HFD groups. The number and size of lung metastases were significantly higher in the HFD group than in the AIN93G group; however, there were no differences in these measurements between the TRF and the AIN93G groups. Time-restricted feeding prevented HFD-induced increases in plasma concentrations of glucose, insulin, proinflammatory cytokines (leptin, monocyte chemotactic protein-1, and plasminogen activator inhibitor-1), and angiogenic factors (angiopoietin-2, hepatic growth factor, and vascular endothelial growth factor). We conclude that TRF attenuates the HFD-enhanced pulmonary metastasis of LLC. This protection may be through the entrainment of metabolic regulators to the fixed feeding time that results in reductions in body adiposity and associated cancer-promoting inflammatory and angiogenic factors. Citation Format: Lin Yan, Sneha Sundaram. Time-restricted feeding attenuates pulmonary metastasis of Lewis lung carcinoma in mice fed a high-fat diet [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1608.

Leptin resensitisation: a reversion of leptin-resistant states.

Leptin resistance refers to states in which leptin fails to promote its anticipated effects, frequently coexisting with hyperleptinaemia. Leptin resistance is closely associated with obesity and also observed in physiological situations such as pregnancy and in seasonal animals. Leptin resensitisation refers to the reversion of leptin-resistant states and is associated with improvement in endocrine and metabolic disturbances commonly observed in obesity and a sustained decrease of plasma leptin levels, possibly below a critical threshold level. In obesity, leptin resensitisation can be achieved with treatments that reduce body adiposity and leptinaemia, or with some pharmacological compounds, while physiological leptin resistance reverts spontaneously. The restoration of leptin sensitivity could be a useful strategy to treat obesity, maintain weight loss and/or reduce the recidivism rate for weight regain after dieting. This review provides an update and discussion about reversion of leptin-resistant states and modulation of the molecular mechanisms involved in each situation.

Recent advances in the understanding and management of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a multifaceted condition characterized by chronic anovulation and excess ovarian activity, in contrast to other causes of anovulation that involve ovarian dormancy or primary insufficiency. Recent studies indicated that PCOS is associated with low-grade chronic inflammation and that women with PCOS are at increased risk of non-alcoholic fatty liver disease. The inflammatory and metabolic derangements associated with PCOS are explained in part by the coexistence of insulin resistance and obesity but are further fueled by the androgen excess. New insights into the regulation of hormones and cytokines in muscle and fat tissue support the concept that PCOS is a systemic syndrome. The therapeutic plan should be tailored to the patient phenotype, complaints, and reproductive desire. Of note, the aromatase inhibitor letrozole seems to be more effective than the reference drug clomiphene citrate to treat infertility due to PCOS. Integral management by a multidisciplinary team may help the patients to adhere to lifestyle interventions and thereby reduce body adiposity and recover their metabolic and reproductive health.

IMPACT OF HIGH-INTENSITY INTERVAL TRAINING ON CENTRAL OBESITY IN OUTPATIENT CARDIAC REHABILITATION PATIENTS WITH METABOLIC SYNDROME

High-intensity interval training (HIIT) is more effective at reducing body adiposity than moderate intensity continuous training (MICT) in overweight individuals. The present study examined the efficacy of HIIT on body composition in cardiac rehabilitation (CR) patients with metabolic syndrome (MetS

Strength training and aerobic exercise alter mitochondrial parameters in brown adipose tissue and equally reduce body adiposity in aged rats.

With aging, there is a reduction in mitochondrial activity, and several changes occur in the body composition, including increased adiposity. The dysfunction of mitochondrial activity causes changes and adaptations in tissue catabolic characteristics. Among them, we can mention brown adipose tissue (BAT). BAT's main function is lipid oxidation for heat production, hence playing a role in adaptive thermogenesis induced by environmental factors such as exercise. It is known that exercise causes a series of metabolic changes, including loss body fat; however, there is still no consensus in the academic community about whether both strength and aerobic exercise equally reduces adiposity. Therefore, this study aimed to evaluate the effects of strength training and aerobic exercise regimes on adiposity, proteins regulating mitochondrial activity, and respiratory complexes in BAT of old rats. The rats were divided in two control groups: young control (YC; N = 5), and old control (OC; N = 5), and two exercise groups: strength training (OST; N = 5), and aerobic treadmill training (OAT; N = 5). Rats were subjected to an 8-week exercise regime, and their body composition parameters were evaluated (total body weight, adiposity index, and BAT weight). In addition, mitochondrial biogenesis proteins (PGC-1α, SIRT1, and pAMPK) and respiratory chain activity (complexes I, II/III, III, and IV) were evaluated. Results showed that OST and OAT exercise protocols significantly increased the mitochondrial regulatory molecules and respiratory chain activity, while body fat percentage and adiposity index significantly decreased. Taken together, both OST and OAT exercise increased BAT weight, activity of respiratory complexes, and regulatory proteins in BAT and equally reduced body adiposity.