2024 UPDATE: the Brazilian Diabetes Society position on the management of metabolic dysfunction-associated steatotic liver disease (MASLD) in people with prediabetes or type 2 diabetes.

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease affecting 30% of the world's population and is often associated with metabolic disorders such as metabolic syndrome, type 2 diabetes (T2D), and cardiovascular disease. This review is an update of the Brazilian Diabetes Society (Sociedade Brasileira de Diabetes [SBD]) evidence-based guideline for the management of MASLD in clinical practice. METHODS: The methodology was published previously and was defined by the internal institutional steering committee. The SBD Metabolic Syndrome and Prediabetes Department drafted the manuscript, selecting key clinical questions for a narrative review using MEDLINE via PubMed with the MeSH terms [diabetes] and [fatty liver]. The best available evidence was reviewed, including randomized clinical trials (RCTs), meta-analyses, and high-quality observational studies related to MASLD. RESULTS AND CONCLUSIONS: The SBD Metabolic Syndrome and Prediabetes Department formulated 9 recommendations for the management of MASLD in people with prediabetes or T2D. Screening for the risk of advanced fibrosis associated with MASLD is recommended in all adults with prediabetes or T2D. Lifestyle modification (LSM) focusing on a reduction in body weight of at least 5% is recommended as the first choice for these patients. In situations where LSMs are insufficient to achieve weight loss, the use of anti-obesity medications is recommended for those with a body mass index (BMI) ≥ 27 kg/m2. Pioglitazone and glucagon-like peptide-1 receptor agonists (GLP-1RA) monotherapy are the first-line pharmacological treatments for steatohepatitis in people with T2D, and sodium-glucose cotransporter-2 (SGLT2) inhibitors may be considered in this context. The combination of these agents may be considered in the treatment of steatohepatitis and/or fibrosis, and bariatric surgery should be considered in patients with a BMI ≥ 35 kg/m2, in which the combination of LSM and pharmacotherapy has not been shown to be effective in improving MASLD.

Gestational and neonatal outcomes of women with partial Dunnigan lipodystrophy.

Introduction: Lipodystrophies are a group of disorders characterized by selective and variable loss of adipose tissue, which can result in an increased risk of insulin resistance and its associated complications. Women with lipodystrophy often have a high frequency of polycystic ovary syndrome (PCOS) and may experience gynecological and obstetric complications. The objective of this study was to describe the gestational outcomes of patients with familial partial lipodystrophy type 2 (FPLD2) at a reference center with the aim of improving the understanding and management of pregnant women affected by this condition. Methods: This was a retrospective analysis of data obtained from questionnaires regarding past pregnancies and a review of medical records from the beginning of follow-up in outpatient clinics. Results: All women diagnosed with FPLD2 who had previously become pregnant were included in this study (n=8). The women in the study experienced pregnancies between the ages of 14 and 38 years, with an average of 1.75 children per woman. The pregnancies in question were either the result of successful conception within 12 months of attempting to conceive or unplanned pregnancies. During pregnancy, two women (25%) were diagnosed with gestational diabetes mellitus (GDM), one (12.5%) with gestational hypothyroidism, and one (12.5%) with preeclampsia. Among the 17 pregnancies, two miscarriages (11.8%) occurred, and five cases (29.4%) of macrosomia were observed. Four instances of premature birth and an equal number of neonatal hypoglycemia cases were recorded. The reported neonatal complications included an unspecified malformation, respiratory infection, and two neonatal deaths related to heart malformation and respiratory distress syndrome. Conclusion: Our data showed a high frequency of fetal complications in women with FPLD2. However, no instances of infertility or prolonged attempts to conceive have been reported, highlighting the significance of employing effective contraception strategies to plan pregnancies at optimal times for managing metabolic comorbidities.

Comprehensive analysis of morbidity and mortality patterns in familial partial lipodystrophy patients: insights from a population study.

Background: There is a lack of information on the clinical and molecular presentation of familial partial lipodystrophy (FPLD), a rare genetic disorder characterized by partial subcutaneous fat loss. Objective: This study aimed to provide a comprehensive assessment of the clinical, metabolic, and genetic features of FPLD in the Brazilian population. Methods: In a multicenter cross-sectional investigation we evaluated patients with FPLD across five Brazilian reference centers for lipodystrophies. Diagnosis of FPLD was made by clinical evaluation and genetic confirmation. Data on genetic, clinical, and metabolic characteristics were captured. Statistical analysis involved the utilization of the Kruskal-Wallis test to identify differences. Results: The study included 106 patients with genetic confirmation of FPLD. The mean age was 44 ± 15 years, and they were predominantly female (78.3%). LMNA pathogenic variants were identified in 85.8% of patients, PPARG in 10.4%, PLIN1 in 2.8%, and MFN2 in 0.9%. Diabetes mellitus (DM) was highly prevalent (57.5%), affecting 54 females (50.9%). Median triglycerides levels were 199 mg/dL (54-2724 mg/dL), severe hypertriglyceridemia (≥ 500 mg/dL) was found in 34.9% and pancreatitis in 8.5%. Metabolic-associated fatty liver disease (MAFLD) was observed in 56.6%, and cardiovascular disease in 10.4%. The overall mortality rate was 3.8%, due to cardiovascular events. Conclusion: This study presents an extensive cohort of Brazilian patients with FPLD, predominantly DM with several multisystem complications. A comprehensive characterization of lipodystrophy syndromes is crucial for effective patient management and care.

Waist circumference is independently associated with liver steatosis and fibrosis in LMNA-related and unrelated Familial Partial Lipodystrophy women.

BACKGROUND: Lipodystrophies are a heterogeneous group of diseases characterized by the selective loss of subcutaneous adipose tissue and ectopic fat deposition in different organs, including the liver. This study aimed to determine the frequencies of liver steatosis (LS) and liver fibrosis (LF) in a sample of individuals with LMNA-related and unrelated Familial Partial Lipodystrophy. METHODS: This cross-sectional study included 17 women with LMNA-related FPLD and 15 women with unrelated FPLD. LS and LF were assessed using transient elastography (TE) with FibroScan®. Anthropometric and biochemical variables were included in a multiple linear regression analysis to identify the variables that were independently related to liver disease. RESULTS: Regarding the presence of LF, 22 (68.2%) women were classified as having non-significant fibrosis, and 10 (31.8%) were classified as having significant or severe fibrosis. Regarding LS, only six women (20.7%) were classified as having an absence of steatosis, and 23 (79.3%) had mild to severe steatosis. After multiple linear regression, waist circumference (but not age, body mass index, or waist-to-hip ratio) was found to be independently related to LS and LF. Among the biochemical variables, only triglyceride levels were independently related to LS but not LF. CONCLUSIONS: In women with FPLD, visceral fat accumulation appears to be the most important determinant of liver disease, including LF, rather than fat scarcity in the lower limbs.

Insulin resistance in obesity and metabolic syndrome: is there a connection with platelet l-arginine transport?

OBJECTIVE: Nitric oxide (NO) is a short-lived gaseous messenger with multiple physiological functions including regulation of blood flow, platelet adhesion and aggregation inhibition. NO synthases (NOS) catalyze the conversion of cationic amino acid L-arginine in L-citrulline and NO. Despite an increasing prevalence of obesity and metabolic syndrome (MetS) in the last decades, the exact mechanisms involved in the pathogenesis and cardiovascular complications are not fully understood. We have examined the effects of obesity and MetS on the L-arginine-NO-cGMP pathway in platelets from a population of adolescents. MATERIALS: A total of twenty six adolescent patients (13 with obesity and 13 with MetS) and healthy volunteers (n=14) participated in this study. Transport of L-arginine, NO synthase (NOS) activity and cGMP content in platelets were analyzed. Moreover, platelet function, plasma levels of L-arginine, metabolic and clinical markers were investigated in these patients and controls. RESULTS: L-arginine transport (pmol/10(9) cells/min) in platelets via system y(+)L was diminished in obese subjects (20.8±4.7, n=10) and MetS patients (18.4±3.8, n=10) compared to controls (52.3±14.8, n=10). The y(+)L transport system correlated negatively to insulin levels and Homeostasis Model Assessment of Insulin Resistance (HOMA IR) index. No differences in NOS activity and cGMP content were found among the groups. Moreover, plasma levels of L-arginine were not affected by obesity or MetS. DISCUSSION: Our study provides the first evidence that obesity and MetS lead to a dysfunction of L-arginine influx, which negatively correlates to insulin resistance. These findings could be a premature marker of future cardiovascular complications during adulthood.

NAFLD as a continuum: from obesity to metabolic syndrome and diabetes.

BACKGROUND: The prevalence of non-alcoholic fatty liver disease (NAFLD) has been increasing rapidly. It is nowadays recognized as the most frequent liver disease, affecting a quarter of global population and regularly coexisting with metabolic disorders such as type 2 diabetes, hypertension, obesity, and cardiovascular disease. In a more simplistic view, NAFLD could be defined as an increase in liver fat content, in the absence of secondary cause of steatosis. In fact, the clinical onset of the disease is a much more complex process, closely related to insulin resistance, limited expandability and dysfunctionality of adipose tissue. A fatty liver is a main driver for a new recognized liver-pancreatic α-cell axis and increased glucagon, contributing to diabetes pathophysiology. MAIN TEXT: This review will focus on the clinical and pathophysiological connections between NAFLD, insulin resistance and type 2 diabetes. We reviewed non-invasive methods and several scoring systems for estimative of steatosis and fibrosis, proposing a multistep process for NAFLD evaluation. We will also discuss treatment options with a more comprehensive view, focusing on the current available therapies for obesity and/or type 2 diabetes that impact each stage of NAFLD. CONCLUSION: The proper understanding of NAFLD spectrum-as a continuum from obesity to metabolic syndrome and diabetes-may contribute to the early identification and for establishment of targeted treatment.

Central-to-peripheral fat ratio, but not peripheral body fat, is related to insulin resistance and androgen markers in polycystic ovary syndrome.

BACKGROUND: Overweight, hyperandrogenism and insulin resistance are cardinal features of patients with polycystic ovary syndrome (PCOS). Women with PCOS have excess accumulation of trunkal fat and metabolic complications. Recent findings suggest that peripheral fat may have metabolic protective behaviour. The aim of this study was to investigate body fat distribution in patients with PCOS and associations of peripheral fat with metabolic and hormonal profile. METHODS: The study included 24 patients with PCOS and a control group of 13 women. Anthropometrical evaluation and dual-energy X-ray absorptiometry to determine body composition was performed. Plasma metabolic and hormonal profiles were evaluated. RESULTS: Patients with PCOS have increased proportion of central to peripheral fat ratio (CPFR) when compared to controls (p = 0.008). There was a positive correlation among trunkal fat, insulin, HOMA-IR and triglycerides (all p < 0.05). Regarding to peripheral fat there was no difference between groups, a trend to negative correlation to insulin appeared. Positive correlation between free androgens index and CPFR (p = 0.058) and a negative correlation between SHBG and CPFR (p = 0.016) were appeared. CONCLUSIONS: Patients with PCOS showed an android pattern fat distribution when compared to controls. Peripheral fat contribution and its relations to androgens in this context could not be established. Android pattern of fat distribution showed inverse correlation to SHBG levels, suggesting that SHBG may be related to fat distribution.

DPP4 activity is related to body weight and central fat in postmenopausal women.

AIMS: Dipeptidyl peptidase-4 (DPP4) is a new adipokine increased in central obesity and related to insulin resistance (IR). Postmenopausal (PM) state may be associated with increase in body weight and central fat distribution. We hypothesize that DPP4 is increased in PM women. MATERIALS AND METHODS: Twenty-two non-obese PM and 22 non-obese premenopausal women (PreM), were evaluated. DPP4 activity, lipid profile, HbA1c, FSH, estradiol and sex hormone-binding globulin (SHBG) were measured; an oral glucose tolerance test (OGTT) was performed and IR calculated. Body composition was assessed by dual X-ray absorptiometry (DXA). Correlations between DPP4 and the anthropometric and metabolic variables and body fat distribution were studied. RESULTS: DPP4 activity was not different between the two groups (PM 5309 ±â€¯650 vs PreM 5387 ±â€¯704 RLU; p = 0,70). In the PM group there was a significant correlation between DPP4 and body weight (r = 0,498; p = 0,03; n = 22) and trunk fat (r = 0,477; p = 0,03; n = 21). There was also a trend for correlation with android (r = 0,418; p = 0,06; n = 21) and total fat (r = 0,409; p = 0,06; n = 21). When stratified by BMI, DPP4 was significantly higher in PM women with BMI ≥25 kg/m2 (p = 0,02). CONCLUSION: DPP4 was not increased in PM but is associated with body weight and body fat centralization.

Pancreatic fat deposition is increased and related to beta-cell function in women with familial partial lipodystrophy.

BACKGROUND: To study pancreatic fat deposition and beta-cell function in familial partial lipodystrophy (FPLD) patients. METHODS: In a cross-sectional study, eleven patients with FPLD, and eight healthy volunteers were matched for age and body mass index and studied at a referral center. Body composition was assessed using dual-energy X-ray absorptiometry and the Dixon method of magnetic resonance imaging was used to quantify pancreatic and liver fat. Fasting plasma glucose, insulin, leptin, lipids and homeostasis model assessment of insulin resistance values were measured, and an oral glucose tolerance test was performed. The insulinogenic index, Matsuda insulin sensitivity index and beta-cell disposition index were calculated. RESULTS: The FPLD group presented a higher waist-to-hip ratio and fat mass ratio and lower total, truncal and lower-limb fat masses. Pancreatic and liver fat contents (log transformed) were significantly higher in the FPLD group (5.26 ± 1.5 vs. 4.08 ± 0.64, p = 0.034 and 0.77 ± 0.50 vs. 0.41 ± 0.18, p = 0.056, respectively). Pancreatic fat was inversely related to the DI (r = - 0.53, p = 0.027) and HDL-cholesterol (r = - 0.63, p = 0.003) and directly related to WHR (r = 0.60; p = 0.009), HbA1c (r = 0.58; p = 0.01) and serum triglyceride (r = 0.48, p = 0.034). Higher triglyceride and lower HDL-cholesterol levels were observed in the FPLD group. CONCLUSIONS: This study demonstrated for the first time that pancreatic fat deposition is increased in FPLD. Moreover, an inverse relationship was demonstrated between pancreatic fat and beta-cell function. The findings of this study may be consistent with the expandability hypothesis and the twin cycle hypothesis.

Is DPP4 activity increased in PCOS?

AIMS: Dipeptidyl peptidase-4 (DPP4) is an adipokine with greater expression in visceral fat and related with insulin resistance (IR). Polycystic ovary syndrome (PCOS) is also associated with IR. Our study aims to evaluate DPP4 activity in PCOS. MATERIALS AND METHODS: Thirty PCOS patients were compared to 28 healthy women. Body composition by dual X-ray absorptiometry (DXA), plasma activity of DPP4 and biochemical variables were performed. All participants underwent an oral glucose tolerance test for insulin and glucose analysis. RESULTS: DPP4 activity was similar in both groups (PCOS 5823 ±â€¯926 vs Control 5501.8 ±â€¯975; p = 0.20). PCOS patients were more IR with lower levels of SHBG (32 vs 47, p = 0.02) and Matsuda index (15.6 vs 20.4, p = 0.03) and higher HOMA-IR (2.8 vs 1.7, p < 0.01), in addition to increased levels of testosterone (55 vs 25, p < 0.01). DPP4 was correlated to HbA1c (r = 0.279, p = 0.03), HDL-c (r = -0.28, p = 0.03) and SHBG (r = -0.256, p = 0.05). CONCLUSIONS: Although PCOS was well characterized as IR and hyperandrogenic, DPP4 was not different in this group. However, a relationship between DPP4 and markers of IR were found. More studies are warranted.

A Novel Generalized Lipodystrophy-Associated Progeroid Syndrome Due to Recurrent Heterozygous LMNA p.T10I Mutation.

Background: Lamin A/C (LMNA) gene mutations cause a heterogeneous group of progeroid disorders, including Hutchinson-Gilford progeria syndrome, mandibuloacral dysplasia, and atypical progeroid syndrome (APS). Five of the 31 previously reported patients with APS harbored a recurrent de novo heterozygous LMNA p.T10I mutation. All five had generalized lipodystrophy, as well as similar metabolic and clinical features, suggesting a distinct progeroid syndrome. Methods: We report nine new patients and follow-up of two previously reported patients with the heterozygous LMNA p.T10I mutation and compare their clinical and metabolic features with other patients with APS. Results: Compared with other patients with APS, those with the heterozygous LMNA p.T10I mutation were younger in age but had increased prevalence of generalized lipodystrophy, diabetes mellitus, acanthosis nigricans, hypertriglyceridemia, and hepatomegaly, together with higher fasting serum insulin and triglyceride levels and lower serum leptin and high-density lipoprotein cholesterol levels. Prominent clinical features included mottled skin pigmentation, joint contractures, and cardiomyopathy resulting in cardiac transplants in three patients at ages 13, 33, and 47 years. Seven patients received metreleptin therapy for 0.5 to 16 years with all, except one noncompliant patient, showing marked improvement in metabolic complications. Conclusions: Patients with the heterozygous LMNA p.T10I mutation have distinct clinical features and significantly worse metabolic complications compared with other patients with APS as well as patients with Hutchinson-Gilford progeria syndrome. We propose that they be recognized as having generalized lipodystrophy-associated progeroid syndrome. Patients with generalized lipodystrophy-associated progeroid syndrome should undergo careful multisystem assessment at onset and yearly metabolic and cardiac evaluation, as hyperglycemia, hypertriglyceridemia, hepatic steatosis, and cardiomyopathy are the major contributors to morbidity and mortality.

Dipeptidyl peptidase-4 levels are increased and partially related to body fat distribution in patients with familial partial lipodystrophy type 2.

BACKGROUND: Dipeptidyl peptidase-4 (DDP4) is an enzyme responsible for glucagon-like peptide-1 inactivation and plays an important role in glucose metabolism. OBJECTIVE: The aim of this study was to evaluate DPP4 levels in patients with familial partial lipodystrophy type 2 (FPLD2) and correlate it with body fat distribution. METHODS: Fourteen patients with FPLD2 were selected to participate in this study and matched to a healthy control group (n = 8). All participants had anthropometrical data registered. Body adiposity index (BAI) was used to evaluate fat distribution in this population. Body fat content and distribution were analyzed by dual X-ray absorptiometry (DXA). Biochemical exams, including DPP4 levels, were performed in all individuals. RESULTS: Despite the same body mass index, lipodystrophic patients had a significant lower hip (median 92.0 vs 94.5; p = 0.028), HDL cholesterol (42.6 ± 10.4 vs 66.1 ± 16.0; p < 0.01) and BAI (24.1 ± 2.8 vs 29.0 ± 3.7; p = 0.02), suggesting that BAI was able to catch differences in fat distribution between groups. On the other hand, patients with FPLD2 presented significant higher levels of insulin (median 11.2 vs 5.3; p = 0.015), triglycerides (184.9 ± 75.4 vs 89.1 ± 51.0; p < 0.01) and DPP4 (4.89 ± 0.92 vs 3.93 ± 1.08; p = 0.04). A trend toward an inverse statistical significance was observed between DPP4 levels and BAI (r = -0.38; p = 0.072). In the lipodistrophic group, a significant correlation was found between DPP4 levels and percentage of total body fat (r = 0.86; p = 0.0025) and android fat (r = 0.78; p = 0.014). CONCLUSIONS: Patients with FPLD2 exhibit an increase in DDP4 levels in comparison to a healthy control group. The increase in the levels of this enzyme does not seem to be related to the diagnosis of diabetes and might be associated with an increase in central fat (estimated using BAI and measured using DXA). These results might be used to reinforce the concept that DDP4 is an adipokine related to central fat distribution.

Relationship between adipokines, inflammation, and vascular reactivity in lean controls and obese subjects with metabolic syndrome.

PURPOSE: Metabolic syndrome is an important risk factor for cardiovascular disease. Adipokines interfere with insulin action and endothelial cell function. We investigated the relationship among adipokines, metabolic factors, inflammatory markers, and vascular reactivity in obese subjects with metabolic syndrome and lean controls. METHODS: Cross-sectional study of 19 obese subjects with metabolic syndrome and 8 lean volunteers evaluated as controls. Vascular reactivity was assessed by venous occlusion pletysmography measuring braquial forearm blood flow (FBF) and vascular resistance (VR) responses to intra-arterial infusions of endothelium-dependent (acetylcholine-Ach) and independent (sodium nitroprusside-SNP) vasodilators. Blood samples were obtained to evaluate C reactive protein (CRP), plasminogen activator inhibitor 1 (PAI-1), fibrinogen, adiponectin, resistin, and lipid profile. Patients were classified with regard to insulin resistance through the HOMA-IR index. RESULTS: PAI-1, CRP and fibrinogen were higher and adiponectin was lower in metabolic syndrome subjects compared to controls. Metabolic syndrome subjects had impaired vascular reactivity. Adiponectin and PAI-1 were associated with insulin, HOMA-IR, triglycerides, and HDLc; and resistin with CRP. Adiponectin was associated with VR after Ach in the pooled group and resistin with D FBF after Ach in the metabolic syndrome group. CONCLUSION: Metabolic syndrome subjects exhibited low levels of adiponectin and high levels of CRP, fibrinogen, and PAI-1. Adiponectin and PAI-1 correlated with insulin resistance markers. Adiponectin and resistin correlated with vascular reactivity parameters. An adipocyte-endothelium interaction might be an important mechanism of inflammation and vascular dysfunction.

[Effects of rosiglitazone on endothelial function in non-diabetic subjects with metabolic syndrome]. / Efeitos da rosiglitazona sobre a função endotelial em indivíduos não-diabéticos com síndrome metabólica.

OBJECTIVE: To evaluate the effects of rosiglitazone (ROSI), an insulin-sensitizer, on endothelial function and endothelial activation markers in a group of non-diabetic subjects with metabolic syndrome. METHODS: A group of eighteen subjects (12 women, 6 men), mean age 41.2 +/- 9.7 and BMI 37.8 +/- 6.1 Kg/m2, was treated with rosiglitazone 8 mg/day for 12 weeks. Another group of nine healthy subjects, mean age 26.1 +/- 4.4 and BMI 21.7 +/- 1.7 Kg/m2, was studied at baseline to compare vasodilator response. Endothelial function was evaluated by venous occlusion plethysmography after intra-arterial infusions of acetylcholine (Ach) and sodium nitroprusside (SNP). The following were measured: glucose, insulin, lipids, fibrinogen, and high-sensitivity C-reactive protein (CRP). HOMA and Quicki indexes were calculated to quantify insulin resistance (IR). RESULTS: There was an improvement in insulin resistance, as evidenced by lower HOMA-R and higher QUICKI index, as well as a decrease in CRP and fibrinogen levels. Endothelium-dependent vasodilation also improved, as evidenced by greater increment in blood flow after Ach and greater decrement in vascular resistance. No difference in endothelium-independent vasodilation was noted. CONCLUSION: Rosiglitazone treatment reduced insulin resistance, fibrinogen, and CRP levels and improved endothelial function in non-diabetic subjects with metabolic syndrome. These data suggest that rosiglitazone plays a role in the regulation of endothelial function in patients at high cardiovascular risk.

[The endocannabinoid system: a new paradigm in the metabolic syndrome treatment]. / O sistema endocanabinóide: novo paradigma no tratamento da síndrome metabólica.

Energetic balance is a fundamental homeostasis mechanism, which contributes to the species' survival. The endocannabinoid system is a new and important component among such mechanisms. Its receptors and endogenous agonists are expressed in central nervous system (CNS) and at various peripheral organs, establishing a CNS-periphery net communication. A relevant aspect is its expression in the adipose tissue, where it regulates lipogenesis and increases the expression of influent genes on lipids and carbohydrate metabolism. Interestingly, it seems to be upregulated in human and animal obesity, although it is activated on demand and rapidly deactivated. Its activation increases food intake and promotes weight gain, contributing to Metabolic Syndrome (MS). Rimonabant is a specific antagonist to the main endocannabinoid receptor (CB1). In animal models of obesity and MS, as well as in humans, Rimonabant has demonstrated to be a useful tool in controlling weight and metabolic aspects. Indeed, some new human trials suggest a possible role for this substance in controlling cardiovascular risk factors related to MS.

Impact of a 6-month treatment with intragastric balloon on body composition and psychopathological profile in obese individuals with metabolic syndrome.

BACKGROUND: The aim of this study was to investigate the effects of a 6-month treatment with intragastric balloon (IGB) on body composition and depressive/anxiety symptoms in obese individuals with metabolic syndrome (MS). METHODS: Fifty patients (aged 18-50 years) with obesity and MS were selected for treatment with IGB for 6 months. Body composition was verified with dual-energy X-ray absorptiometry (DXA) at baseline and right after IGB removal. Anxiety/depressive symptoms were assessed with the Beck Depression Inventory (BDI) and the hospital anxiety and depression scale (HADS) at baseline and after 6 months of treatment. RESULTS: In total, 39 patients completed the study. After 6 months, there were significant decreases in weight (11.7 ± 9.6 kg, p < 0.0001) and waist circumference (9.3 ± 8.2 cm, p < 0.0001). Weight loss was also demonstrated by DXA and corresponded to decreases of 3.0 ± 3.4% in body fat percentage, 7.53 ± 7.62 kg in total body fat, and 3.70 ± 4.89 kg in lean body mass (p < 0.001 for all comparisons). Depressive symptoms scores decreased by a mean of 4.57 ± 10.6 points when assessed with the BDI (p = 0.002) and 1.82 ± 5.16 points when assessed with the HADS-Depression (p = 0.0345). Anxiety symptoms scores decreased by a mean of 1.84 ± 4.04 points when determined with the HADS-anxiety (p = 0.0066). The decrease in body fat percentage was the parameter that best correlated with improvements in depressive (p = 0.008) and anxiety symptoms (p = 0.014). CONCLUSIONS: In obese individuals with MS, fat mass reduction was associated with short-term improvements in depressive and anxiety symptoms. Trial Registration Registered at ClinicalTrials.gov, NCT01598233.

[Evaluation of the sibutramine effect on satiety with a visual analogue scale in obese adolescents]. / Avaliação do efeito da sibutramina sobre a saciedade por escala visual analógica em adolescentes obesos.

Initially used to measure algic symptoms, visual analogue scales (VAS) can also be useful for the evaluation of satiety. The antiobesity agent sibutramine, unlike anorectic agents, decreases food intake mainly by stimulating satiety. To evaluate the effect of sibutramine on satiety, we used a VAS in obese adolescents participating in a double-blind, randomized trial comparing 10 mg of sibutramine to placebo. Each patient received 13 scales to be checked at hourly intervals, in a single day, from 9 am to 9 pm. A 500 kcal deficit diet was divided into 3 meals, with previously fixed times: 9:30 h, 12:30 h, 18:30 h. Using the scores obtained from each scale, a line graph was designed to represent the average satiety score throughout the day. Comparing the area under the curve for the 2 groups, we found 4.609 +/- 1.309 for the group treated with sibutramine and 4.141 +/- 1.432 for the placebo group, not reaching statistical significance (p= NS). Therefore, sibutramine does not seem do have an effect on satiety of obese adolescents, at least when satiety is evaluated by a VAS.

Erratum: Body composition study by dual-energy x-ray absorptiometry in familial partial lipodystrophy: finding new tools for an objective evaluation.

[This corrects the article DOI: 10.1186/1758-5996-4-40.].

The role of glucagon on type 2 diabetes at a glance.

The opposite effects of insulin and glucagon in fuel homeostasis, the paracrine/endocrine inhibitory effects of insulin on glucagon secretion and the hyperglucagonemia in the pathogenesis of type 2 diabetes (T2D) have long been recognized. Inappropriately increased alpha-cell function importantly contributes to hyperglycemia and reflects the loss of tonic restraint normally exerted by high local concentrations of insulin on alpha-cells, possibly as a result of beta-cell failure and alpha-cell insulin resistance, but additional mechanisms, such as the participation of incretin hormones in this response, have also been suggested. Three classes of drugs already available for clinical use address the abnormalities of glucagon secretion in T2D, namely, the GLP-1 receptor agonists (GLP-1RA), the inhibitors of dipeptidyl peptidase-4 (DPP-4i) and the amylin agonist pramlintide; it has been proposed that the glucagonostatic and insulinotropic effects of GLP-1RA equally contribute to their hypoglycemic efficacy. In this review, the control of glucagon secretion and its participation in T2D pathogenesis are summarized.