Body Fat Mass In Patients Research Articles

Long-Term pemafibrate treatment exhibits limited impact on body fat mass in patients with hypertriglyceridemia accompanying NAFLD.

Short-term use of pemafibrate (PEM), a selective modulator of peroxisome proliferator-activated receptor alpha, has been reported to improve abnormal liver function in patients with nonalcoholic fatty liver disease with hypertriglyceridemia (HTG-NAFLD). This study aimed to clarify the effects and predictive factors of long-term 72-week PEM administration on body composition, and laboratory tests in HTG-NAFLD patients. Fifty-three HTG-NAFLD patients receiving a 72-week PEM regimen were retrospectively enrolled. Routine blood and body composition results were analyzed immediately before and at the end of the study period. PEM treatment significantly improved liver enzyme levels such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and gamma-glutamyl transferase, along with lipid profiles including triglyceride, total cholesterol, and low-density lipoprotein cholesterol. PEM did not have any detectable impact on body composition parameters. The factors of female, higher AST (≥ 46 U/L) and fat mass (≥ 31.9%), as well as lower soft lean mass (< 61.6%), skeletal muscle mass (< 36%), and skeletal muscle mass index (< 6.9 kg/m2) were significantly associated with the treatment response status of a > 30% decrease in ALT. All patients completed the treatment without any adverse effects. Long-term PEM treatment had a positive impact on liver enzymes and lipid profiles, but it did not result in significant changes in body composition among HTG-NAFLD patients. In predicting the response to PEM treatment, the evaluation of AST and body composition may be useful.

Effects of Changes in Body Fat Mass as a Result of Regular Exercise on Hemoglobin A1c in Patients With Type 2 Diabetes Mellitus: A Meta-Analysis.

An increase in visceral fat is associated with an increase in insulin resistance, so reducing body fat mass through exercise may help alleviate type 2 diabetes mellitus (T2DM). The current meta-analysis evaluated the effect of changes in body fat via an intervention of regular exercise on hemoglobin A1c (HbA1c) in patients with T2DM. The inclusion criteria were randomized controlled trials involving adults with T2DM, intervention involving exercise alone, an overall duration of intervention ≥12weeks, and reporting HbA1c and body fat mass. The mean differences (MDs) were defined as the MD between the exercise group and the control group, and the MDs in HbA1c (in percentage) and body fat mass (in kilograms) were calculated. All MDs in HbA1c were pooled as overall effects. A meta-regression analysis was performed to evaluate the relationship between the MD in the body fat mass (in kilograms) and the MD in HbA1c. Twenty studies (1,134 subjects) were analyzed. The pooled MD in HbA1c (in percentage) decreased significantly (-0.4; 95% confidence interval [-0.5, -0.3]) but contained significant heterogeneity (Q = 52.7, p < .01; I2 = 41.6%). A meta-regression analysis showed that a decrease in the MD in body fat mass was significantly associated with a decrease in the MD in HbA1c (R2 = 80.0%) and heterogeneity decreased (Q = 27.3, p = .61; I2 = 11.9%), and a reduction in body fat mass of 1kg was estimated to decrease the HbA1c (%) by approximately 0.2. The current study suggested that a decrease in HbA1c due to regular exercise depends on a reduction in body fat mass in patients with T2DM.

Relationships among Postprandial Plasma Active GLP-1 and GIP Excursions, Skeletal Muscle Mass, and Body Fat Mass in Patients with Type 2 Diabetes Treated with Either Miglitol, Sitagliptin, or Their Combination: A Secondary Analysis of the MASTER Study.

We previously conducted a pilot randomized controlled trial "the MASTER study" and demonstrated that alpha-glucosidase inhibitor miglitol and a dipeptidyl peptidase-4 inhibitor sitagliptin modified postprandial plasma excursions of active glucagon-like peptide-1 (aGLP-1) and active gastric inhibitory polypeptide (aGIP), and miglitol treatment decreased body fat mass in patients with type 2 diabetes (T2D). However, the details regarding the relationships among postprandial plasma aGLP-1 and aGIP excursions, skeletal muscle mass, and body fat mass are unclear. We conducted a secondary analysis of the relationships among skeletal muscle mass index (SMI), total body fat mass index (TBFMI), and the incremental area under the curves (iAUC) of plasma aGLP-1 and aGIP excursions following mixed meal ingestion at baseline and after 24-week add-on treatment with either miglitol alone, sitagliptin alone, or their combination in T2D patients. SMI was not changed after the 24-week treatment with miglitol and/or sitagliptin. TBFMI was reduced and the rates of aGIP-iAUC change were lowered in the two groups treated with miglitol, although their correlations did not reach statistical significance. We observed a positive correlation between the rates of aGIP-iAUC and TBFMI changes and a negative correlation between the rates of TBFMI and SMI changes in T2D patients treated with sitagliptin alone whose rates of aGIP-iAUC change were elevated. Collectively, although T2D patients treated with miglitol and/or sitagliptin did not show altered SMI after 24-week treatment, the current study suggests that there are possible interrelationships among postprandial plasma aGIP excursion modified by sitagliptin, skeletal muscle mass, and body fat mass.

Relationship Between Acyl and Desacyl Ghrelin Levels with Insulin Resistance and Body Fat Mass in Type 2 Diabetes Mellitus.

PurposeAlthough strong evidence suggests that ghrelin plays an important role in regulating energy balance, the effects of acylated ghrelin (AG) and deacylated ghrelin (DAG) on fat mass are largely undefined. This study aimed to investigate the differential associations of both forms of ghrelin with insulin resistance and body fat mass in patients with type 2 diabetes mellitus (T2DM).Patients and MethodsA total of 162 patients with type 2 diabetes were recruited and classified based on BMI and visceral fat area (VFA) as VFA normal group (n = 78), normal-BMI VFA obesity group (n = 20) and high-BMI VFA obesity group (n = 64). VFA and subcutaneous fat area (SFA) were detected by bioelectrical impedance analysis. Blood samples were collected to measure fasting glucose, insulin, lipids, AG and DAG levels after clinical examination.ResultsCompared with VFA normal group, DAG levels were significantly lower (421.7 ± 106.0 and 388.7 ± 96.5 pg/mL vs 524.4 ± 141.5 pg/mL, P < 0.01) in the two VFA obesity groups. No significant difference was found in AG levels within three groups. Among all subjects, BMI, VFA, SFA, fasting insulin and HOMA-IR were negatively correlated with DAG but positively with AG/DAG ratio (P < 0.01). In contrast, AG was positively correlated with HOMA-IR and fasting glucose (P < 0.01). Multiple stepwise regression analysis showed that fasting glucose was the independent factor of AG, VFA and HOMA-IR were the independent factors related to DAG.ConclusionDAG levels have a strong negative association with excess body fat mass and insulin resistance, whereas AG levels are closely related to elevated blood glucose levels in T2DM patients.

Re-evaluation of serum leptin and adiponectin concentrations normalized by body fat mass in patients with rheumatoid arthritis

Leptin and adiponectin are produced mainly in adipocytes and classified as adipocytokines because of their possible involvement in inflammation and immunity. The aim of this study was to elucidate the relationships of these adipocytokines with the disease activities of RA. We examined leptin and adiponectin concentrations and inflammatory markers such as metalloproteinase-3 (MMP-3) in 136 patients with rheumatoid arthritis (RA) (26 males and 110 females, 69.6 ± 9.3 years) and 78 controls (36 males and 42 females, 66.7 ± 15.0 years). Serum leptin and adiponectin concentrations correlated positively (r = 0.565, P < 0.001) and negatively (r = –0.331, P < 0.001) to the amount of body fat, respectively. Serum leptin and adiponectin concentrations normalized by body fat mass were significantly higher in RA than those in controls [leptin, 1.24 (median) ng/mL/kg fat in RA vs. 0.76 ng/mL/kg fat in controls; adiponectin, 0.74 μg/mL/kg fat in RA vs. 0.44 μg/mL/kg fat in controls]. Normalized adiponectin concentrations correlated positively not only to the degree of bone destruction in Steinbrocker classification but also to serum MMP-3 concentrations. Normalized leptin concentrations did not correlate to the degree of bone destruction. We conclude that adiponectin but not leptin may be involved in joint damage in RA.

Nutritional intake and body composition in children with inflammatory bowel disease

AbstractPurposeIn this study we assessed nutritional intake, body composition, and their relationship in patients with paediatric inflammatory bowel disease (IBD).MethodsWe conducted a longitudinal, prospective study of 38 patients' nutritional intake using 3-day food records (FR) and bioimpedance analysis of body composition. FR were evaluated by Nutricomp DietCAD software. Results were analysed with Microsoft Excel 2013 and IBM SPSS Statistics 22 software.ResultsPatients treated with biological and conventional therapy (CT) had a higher intake of vegetable protein and carbohydrate from starch than those treated earlier with exclusive enteral nutrition (EEN) in the remission phase (F = 5.926, F = 5.130, P &lt; 0.05). The former EEN group had a higher intake of iron compared to the other two groups (F = 3.967, P = 0.036). Protein intake and fat-free mass (FFM) had a significant positive correlation, while added sugar correlated with body fat mass (BFM) in the same way (R2 = 0.122, R2 = 0.169, P &lt; 0.05). Body-fat mass in patients of the biological therapy (BT) group overstepped the healthy median, and the FFM in the EEN group stayed under it.ConclusionsOur results confirm that it is essential to monitor body composition and not only measure body weight. Patients should be advised based on their body composition, therapy, and phase of the disease.

Metformin Therapy Reduces Obesity Indices in Children and Adolescents: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Purpose: Few studies have summarized findings for the effect of metformin on obesity indices. Therefore, we aimed to conduct a systematic review and meta-analysis on the effect of metformin on obesity indices among children and adolescents. Methods: Relevant articles published up to September 2018 were searched in SCOPUS, Medline, and Google Scholar using appropriate keywords. All clinical trials that examined the effect of metformin on obesity indices in children and adolescents were included. Results: Overall, 38 studies, including 2199 participants (39.75% male and 60.25% female), were included. The pooled results indicated that metformin significantly reduced BMI [weighted mean difference (WMD): -1.07 kg/m2; 95% confidence interval (CI): -1.43 to -0.72]. Same findings were found for waist circumference (WC) (WMD: -1.93 cm; 95% CI: -2.69 to -1.16). Metformin also reduced body weight in all participants (WMD: -2.51 kg; 95% CI: -3.14 to -1.89). Moreover, it reduced body fat mass in patients with overweight or obesity (WMD: -1.90%; 95% CI: -3.25 to -0.56) and chronic diseases (WMD: -1.41%; 95% CI: -2.23 to -0.58), but not among those with growth problems. Metformin therapy did not affect lean body mass (LBM) in patients with overweight or obesity and growth problems; however, it reduced LBM in patients with chronic diseases (WMD: -1.49 kg; 95% CI: -2.69 to -0.30). Conclusions: We found a significant reduction in BMI, body weight, WC, and fat mass following administration with metformin. However, the effect of metformin on LBM was not significant. Further studies are required to confirm these findings.

1019-P: Glucagon-Like Peptide-1 Receptor Agonists Predominantly Reduce Body Fat Mass in Patients with Type 2 Diabetes

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) helps obese patients with type 2 diabetes (T2DM) lose weight. Because few studies have researched their effectiveness on body composition, this study aimed to investigate the effect of GLP-1 RA on body fat mass (BFM) and skeletal muscle mass (SMM) in patients with T2DM. In this retrospective study, we reviewed the database of our clinic and identified patients who had been prescribed GLP-1 RAs between 2010-2017. Patients who were either switched from insulin, had used any drugs that affect blood glucose levels (except metformin and sulfonylurea), or who had clinically significant disease were excluded. Both baseline and 12-month body compositions were assessed via the BIA device (Inbody S10 or S20). Body weight (BW), body mass index (BMI), and HbA1c were also measured. Data were analyzed using the paired t-test, with values shown as mean±SD. A total of 205 patients were identified and 45 were included in the final analysis; 25 were non-insulin users and 20 were insulin users. After 12-month treatment, HbA1c, BW, and BMI were significantly reduced in both groups (Table 1). Interestingly, while BFM was significantly decreased, no differences in fat free mass or SMM were noted. In conclusion, GLP-1 RA treatment leads to weight loss by predominantly reducing body fat mass in patients with T2DM regardless of being treated or not treated with insulin. Disclosure Y. Fujita: None. S. Kubota: None. H. Kuwata: Research Support; Self; Eli Lilly and Company. D. Yabe: Advisory Panel; Self; Abbott. Research Support; Self; Astellas Pharma Inc. Speaker's Bureau; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Daiichi Sankyo Company, Limited, Eli Lilly and Company, Merck Sharp &amp; Dohme Corp., Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Sanofi K.K., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited. Y. Hamamoto: Speaker's Bureau; Self; Novo Nordisk A/S. Y. Seino: Research Support; Self; Arkray, Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Eli Lilly and Company, Merck &amp; Co., Inc., Novo Nordisk Inc., Ono Pharmaceutical Co., Ltd., Taisho Pharmaceutical Co., Ltd., Takeda Pharmaceutical Company Limited, Terumo Medical Corporation.

Body fat mass in patients with chronic obstructive pulmonary disease as a risk factor for right ventricular structural-functional changes

Aim. To study the correlation between the body fat mass (BFM) and the structural-functional characteristics of right ventricle (RV) in patients with different body mass, suffering from chronic obstructive pulmonary disease (COPD).&#x0D; Materials and methods. Echocardiography, ultrasound determination of subcutaneous and premesenterial layer thickness, assessment of leptin level was performed in 72 COPD patients, who were divided into three groups: group 1 – patients with normal body mass (n = 31), group 2 – patients with excess weight (n = 21), group 3 – patients with class I-II obesity (n= 20).&#x0D; Results. Among COPD patients, body mass index (BMI) growth causes increase in BFM and subcutaneous and premesenterial fat thickness, elevation in blood serum leptin level, but decrease in lean body mass (LBM). The global longitudinal systolic strain of the free wall of RV in COPD patients with obesity (–17.39 ± 3.64, p = 0.002) and elevated body mass (–17.96 ± 5.69, p = 0.006) is reduced.&#x0D; Conclusions. Among COPD patients with different body mass, the global longitudinal systolic strain of RV free wall aggravates as leptin level and body fat mass grow that can be the reflection of mechanical exposure and epicardial fat pressure on the right ventricle.

The SGLT2 Inhibitor Dapagliflozin Significantly Improves the Peripheral Microvascular Endothelial Function in Patients with Uncontrolled Type 2 Diabetes Mellitus.

Objective Sodium-glucose co-transporter 2 (SGLT2) inhibitors reduce cardiovascular events and decrease the body fat mass in patients with type 2 diabetes mellitus (T2DM). We examined whether or not the SGLT2-inhibitor dapagliflozin can improve the endothelial function associated with a reduction in abdominal fat mass. Methods We prospectively recruited patients with uncontrolled [hemoglobin A1c (HbA1c) >7.0%] T2DM who were not being treated by SGLT2 inhibitors. Patients were treated with add-on dapagliflozin (5 mg/day) or non-SGLT2 inhibitor medicines for 6 months to improve their HbA1c. We measured the peripheral microvascular endothelial function as assessed by reactive hyperemia peripheral arterial tonometry (RH-PAT) and calculated the natural logarithmic transformed value of the RH-PAT index (LnRHI). We then investigated changes in the LnRHI and abdominal fat area using computed tomography (CT). Results The subjects were 54 patients with uncontrolled T2DM (72.2% men) with a mean HbA1c of 8.1%. The HbA1c was significantly decreased in both groups, with no significant difference between the groups. Dapagliflozin treatment, but not non-SGLT2 inhibitor treatment, significantly increased the LnRHI. The changes in the LnRHI were significantly greater in the dapagliflozin group than in the non-SGLT2 inhibitor group. Dapagliflozin treatment, but not non-SGLT2 inhibitor treatment, significantly decreased the abdominal visceral fat area, subcutaneous fat area (SFA), and total fat area (TFA) as assessed by CT and significantly increased the plasma adiponectin levels. The percentage changes in the LnRHI were significantly correlated with changes in the SFA, TFA, systolic blood pressure, and adiponectin. Conclusion Add-on treatment with dapagliflozin significantly improves the glycemic control and endothelial function associated with a reduction in the abdominal fat mass in patients with uncontrolled T2DM.

Changes in Body Fat Mass in Patients after Starting Peritoneal Dialysis

Peritoneal dialysis (PD) is characterized by gain in fat mass. Visceral fat mass is associated with metabolic syndrome and atherosclerosis rather than subcutaneous fat mass. In addition, the change in visceral fat mass is a more reliable predictor of survival in PD patients. In this study, we prospectively examined serial changes in fat composition and nutritional status and analyzed factors associated with gain in fat mass in patients undergoing PD. Body composition was assessed by bioelectric impedance analysis (BIA) and computed tomogram (CT). Nutrition status was assessed by Subjective Global Assessment (SGA), protein equivalent of nitrogen appearance (nPNA), serum albumin, C-reactive protein (CRP), and lipid profile. All measurements except BIA were performed on the seventh day and at 6 and 12 months after the start of PD. 60 patients (30 men; mean age 55.0 ± 12.5 years) were enrolled. Increase in body weight continued during the 12 months but visceral and subcutaneous fat mass increased during the first 6 months and decreased during the second 6 months. While hematocrit and serum albumin decreased during the first 6 months, they did not change during the second 6 months. Serum creatinine, total cholesterol, and triglyceride increased similarly to the weight pattern. While nPNA decreased during the 12 months, Kt/V, SGA, and CRP did not change. Patients that had more visceral fat mass at the start of PD had less gain of visceral fat mass during the first 6 months (r = -0.821, p = 0.002). Patients that had more subcutaneous fat mass at the start of PD had less gain of subcutaneous fat mass (r = -0.709, p = 0.015). The change in weight was not associated with the change in visceral or subcutaneous fat during the first 6 months. Patients starting PD experience weight gain, including visceral and subcutaneous fat, during the first 6 months of PD. Patients with high baseline fat mass had less increase in fat mass than those with low baseline fat mass, regardless of visceral or subcutaneous fat mass.

Is Fetuin-A/α2-Heremans-Schmid Glycoprotein Associated with the Metabolic Syndrome in Patients with Chronic Kidney Disease?

Introduction: Components of the metabolic syndrome are highly prevalent in chronic kidney disease (CKD) patients – some of which paradoxically appear to predict an improved outcome in this population. We hypothesized that the circulating calcification inhibitor fetuin-A/AHSG, which is also a natural inhibitor of the tyrosine kinase insulin receptor, could be one factor explaining the association between increased fat mass and a survival advantage in CKD and thus conducted an explorational study to provide preliminary data to support further research into this hypothesis. Patients and Methods: In a cross-sectional study, we evaluated 198 CKD stage 5 patients (GFR 6.8 ± 0.2 ml/min; 62% males, mean age 52 ± 1 years) close to the start of renal replacement therapy. We studied circulating AHSG (ELISA) and two common functional AHSG gene polymorphisms (at amino acids Thr248Met (C-T) and Thr256Ser (C-G) using Pyrosequencing®) and related these to multiple components of the metabolic syndrome. Results: Median circulating AHSG was lower (p < 0.01) in type-2 (0.22 g/l) and type-1 (0.16 g/l) diabetics as compared to non-diabetic CKD-5 patients (0.24 g/l). AHSG correlated with both total and truncal fat mass in type-2 diabetics (rho 0.37 and 0.39; p < 0.001, respectively), but not in type-1 diabetics or non-diabetics. Both SNPs significantly influenced circulating levels of AHSG, and were also associated with significant differences in serum triglycerides and HDL cholesterol. Furthermore, there were significant differences in the prevalence of metabolic syndrome criteria between the AHSG Thr256Ser (C-G) genotype groups, with a more atherogenic lipid profile in AHSG high producers (Thr/Thr homozygotes). In multivariate analysis, the association between circulating AHSG and fat mass remained significant also after adjustment for age, gender, inflammation (CRP >10 mg/l), and AHSG genotype. Conclusions: The present, explorational, study supports further, mechanistic, studies into a physiological link between AHSG and body fat mass in patients with CKD. As we observed an association between higher fat mass and elevated AHSG levels, these preliminary results may form the basis of further study to establish if the observed associations may be one reason why obesity has been reported to constitute a survival advantage in CKD.

The Relation Between Serum Leptin Levels and Body Fat Mass in Patients with Active Lung Tuberculosis

The relationship of leptin to diminished appetite and weight loss has been investigated in many diseases. Diminished appetite and weight loss are the most apparent characteristics of patients with active lung tuberculosis and in this study the relation of leptin to such diminished appetite and weight loss has been investigated in patients with active lung tuberculosis before and after treatment. Twenty‐five patients (7 female, 18 male) with active tuberculosis having an age range of 18–70 years (mean 47.48 ± 15.36 y) and 25 normal individuals (9 female, 16 male) having an age range of 25–71 years (mean 44.60 ± 13.80 y) were included in this study. Leptin levels, body mass index (BMI), body fat ratio (BFR), and waist hip ratio (WHR) were measured before and after 6 months of antituberculosis treatment. The same measurements were also made in the control group and the results were compared. While the pretreatment BMI (22.02 ± 4.31 kg/m2) and BFR (16.60% ± 9.30%) values in the patient group were significantly lower than in the control group, we found no difference in their pretreatment WHR values. Pretreatment leptin levels (3.49 ± 3.34 µg/L) were significantly higher in patients with tuberculosis than in the control group (2.33 ± 1.10 µg/L). Leptin levels were found to be significantly increased at the 6th month of antituberculosis treatment (5.65 ± 5.41 µg/L) than the pretreatment values (p < 0.05). We observed an evident increase in BMI (24.10 ± 4.87 kg/m2) and BFR (17.51% ± 9.25%) due to antituberculosis treatment (p < 0.05). This study suggests that leptin has a role in the diminished appetite and weight loss symptoms in patients with active lung tuberculosis.