scholarly journals Tryptophan Metabolism Is Associated with BMI and Adipose Tissue Mass and Linked to Metabolic Disease in Pediatric Obesity

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 286
Author(s):  
Julia Lischka ◽  
Andrea Schanzer ◽  
Margot Baumgartner ◽  
Charlotte de Gier ◽  
Susanne Greber-Platzer ◽  
...  
Keyword(s):  
Metabolic Disease ◽  
Body Fat ◽  
Fat Mass ◽  
Pediatric Obesity ◽  
Severe Obesity ◽  
Metabolic Diseases ◽  
Tryptophan Metabolism ◽  
Body Fat Mass ◽  
Tissue Mass ◽  
The Impact

The obesity epidemic has contributed to an escalating prevalence of metabolic diseases in children. Overnutrition leads to increased tryptophan uptake and availability. An association between the induction of the tryptophan catabolic pathway via indoleamine 2,3-dioxygenase (IDO) activity and obesity-related inflammation has been observed. This study aimed to investigate the impact of pediatric obesity on tryptophan metabolism and the potential relationship with metabolic disease. In this prospective cohort study, plasma kynurenine, tryptophan, and serotonin levels were measured by ELISA, and IDO activity was estimated by calculating the kynurenine/tryptophan ratio in a clinically characterized population with severe obesity (BMI ≥ 97th percentile) aged 9 to 19 (n = 125). IDO activity and its product kynurenine correlated with BMI z-score and body fat mass, whereas concentrations of serotonin, the alternative tryptophan metabolite, negatively correlated with these measures of adiposity. Kynurenine and tryptophan, but not serotonin levels, were associated with disturbed glucose metabolism. Tryptophan concentrations negatively correlated with adiponectin and were significantly higher in prediabetes and metabolically unhealthy obesity. In conclusion, BMI and body fat mass were associated with increased tryptophan catabolism via the kynurenine pathway and decreased serotonin production in children and adolescents with severe obesity. The resulting elevated kynurenine levels may contribute to metabolic disease in obesity.

scholarly journals The Impact ofLEPG-2548A andLEPRGln223Arg Polymorphisms on Adiposity, Leptin, and Leptin-Receptor Serum Levels in a Mexican Mestizo Population

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Efraín Chavarria-Avila ◽  
Mónica Vázquez-Del Mercado ◽  
Eduardo Gomez-Bañuelos ◽  
Sandra-Luz Ruiz-Quezada ◽  
Jorge Castro-Albarran ◽  
...  
Keyword(s):  
Body Fat ◽  
Fat Mass ◽  
Leptin Receptor ◽  
Serum Levels ◽  
Normal Weight ◽  
Body Fat Mass ◽  
Western Mexico ◽  
Pcr Rflp ◽  
Obese Subjects ◽  
The Impact

The polymorphisms in leptin (LEPG-2548A) and leptin-receptor (LEPRGln223Arg) seem to influence obesity and lipid metabolism among others. The aim of this study was to investigate the effect of these polymorphisms on adiposity, leptin (sLeptin), and leptin-receptor (sLeptin-receptor) serum concentrations as well as inflammation markers. We included 382 adults originally from Western Mexico. They were genotyped by PCR-RFLP. Obese individuals showed higher sLeptin (58.2±31.35 ng/mL) but lower sLeptin-receptor (12.6±3.74 ng/mL) levels than normal weight ones (17.6±14.62 ng/mL,17.4±4.62 ng/mL, resp.),P<0.001. Obese subjects carriers of Arg/Arg genotype had more (P=0.016) sLeptin-receptor (14.7±4.96 ng/mL) and less (P=0.004) sLeptin (44.0±28.12 ng/mL) levels than Gln/Gln genotype (11.0±2.92 ng/mL,80.3±33.24 ng/mL, resp.). Body fat mass was lower (Pfrom 0.003 to 0.045) for A/A (36.5%±6.80) or Arg/Arg (36.8%±6.82) genotypes with respect to G/G (41.3%±5.52) and G/A (41.6%±5.61) or Gln/Gln (43.7%±4.74) and Gln/Arg (41.0%±5.52) genotypes carriers. Our results suggest thatLEP-2548A andLEPR223Arg could be genetic markers of less body fat mass accumulation in obese subjects from Western Mexico.

Carbenoxolone treatment attenuates symptoms of metabolic syndrome and atherogenesis in obese, hyperlipidemic mice

2007 ◽  
Vol 293 (6) ◽  
pp. E1517-E1528 ◽  
Author(s):  
Alli M. Nuotio-Antar ◽  
David L. Hachey ◽  
Alyssa H. Hasty
Keyword(s):  
Risk Factors ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Body Fat ◽  
Fat Mass ◽  
Severe Obesity ◽  
Plasma Lipids ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Body Fat Mass

Glucocorticoids, which are well established to regulate body fat mass distribution, adipocyte lipolysis, hepatic gluconeogenesis, and hepatocyte VLDL secretion, are speculated to play a role in the pathology of metabolic syndrome. Recent focus has been on the activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which is capable of regenerating, and thus amplifying, glucocorticoids in key metabolic tissues such as liver and adipose tissue. To determine the effects of global 11β-HSD1 inhibition on metabolic syndrome risk factors, we subcutaneously injected “Western”-type diet-fed hyperlipidemic mice displaying moderate or severe obesity [LDL receptor (LDLR)-deficient (LDLR−/−) mice and mice derived from heterozygous agouti ( A y /a) and homozygous LDLR−/− breeding pairs ( A y /a;LDLR−/− mice)] with the nonselective 11β-HSD inhibitor carbenoxolone for 4 wk. Body composition throughout the study, end-point fasting plasma, and extent of hepatic steatosis and atherosclerosis were assessed. This route of treatment led to detection of high levels of carbenoxolone in liver and fat and resulted in decreased weight gain due to reduced body fat mass in both mouse models. However, only A y /a;LDLR−/− mice showed an effect of 11β-HSD1 inhibition on fasting insulin and plasma lipids, coincident with a reduction in VLDL due to mildly increased VLDL clearance and dramatically decreased hepatic triglyceride production. A y /a;LDLR−/− mice also showed a greater effect of the drug on reducing atherosclerotic lesion formation. These findings indicate that subcutaneous injection of an 11β-HSD1 inhibitor allows for the targeting of the enzyme in not only liver, but also adipose tissue, and attenuates many metabolic syndrome risk factors, with more pronounced effects in cases of severe obesity and hyperlipidemia.

scholarly journals Association between low-grade chronic inflammation with adipocytokines and body fat mass in superobese male children

2019 ◽  
Vol 59 (1) ◽  
pp. 13-7
Author(s):  
Aryono Hendarto ◽  
Sudigdo Sastroasmoro ◽  
Damayanti Rusli Sjarif
Keyword(s):  
Chronic Inflammation ◽  
Body Fat ◽  
Fat Mass ◽  
Metabolic Diseases ◽  
Low Grade ◽  
Body Fat Mass ◽  
Hscrp Level ◽  
Fat Percentage ◽  
Bioelectric Impedance Analysis ◽  
Tnf Α

Background Obesity causes adipocytokines dysregulation and enhances the pro-inflammatory response. Low-grade chronic inflammation is related to cardiometabolic diseases. Objective To evaluate the status of low-grade chronic inflammation in pre-pubertal, obese boys and its potential correlation to adipocytokines and body fat mass. Methods This cross-sectional study included pre-pubertal, male, superobese children as the subjects. We determined obesity status using the CDC 2000 BMI-for-age chart. Body fat percentage was measured using bioelectric impedance analysis (BIA). Fasting blood specimens were collected to evaluate hsCRP, leptin, adiponectin, and TNF-α levels. Results Eighty subjects were recruited into this study, with a mean age of 6.9 years. Ten subjects (12.5%) had low-grade chronic inflammation (hsCRP level ≥ 1 mg/L). The levels of hsCRP was not correlated with leptin, adiponectin, and TNF-α levels. A weak, but significant correlation was observed between hsCRP level and body fat mass (r= +0.383; P<0.0001). The hsCRP level increased with increasing body fat mass, until it reached its peak at body fat mass of 28 kg. Beyond that point, hsCRP level was stable. Conclusion Low-grade chronic inflammation begins at a young age in obese children. The hsCRP level has a weak correlation with body fat mass, but no correlation with adipocytokine levels. Prevention and treatment of childhood obesity should be prioritized to prevent further cardiovascular and metabolic diseases.

Novel genes on rat chromosome 10 are linked to body fat mass, preadipocyte number and adipocyte size

2016 ◽  
Vol 11 (S 01) ◽  
Author(s):  
A Weingarten ◽  
L Turchetti ◽  
K Krohn ◽  
M Kern ◽  
I Klöting ◽  
...  
Keyword(s):  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Adipocyte Size ◽  
Chromosome 10 ◽  
Novel Genes

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

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1019-P
Author(s):  
YUKI FUJITA ◽  
SODAI KUBOTA ◽  
HITOSHI KUWATA ◽  
DAISUKE YABE ◽  
YOSHIYUKI HAMAMOTO ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Body Fat ◽  
Fat Mass ◽  
Body Fat Mass ◽  
Receptor Agonists ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals High percent body fat mass predicts lower risk of cardiac events in patients with heart failure: an explanation of the obesity paradox

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Katsuhiko Ohori ◽  
Toshiyuki Yano ◽  
Satoshi Katano ◽  
Hidemichi Kouzu ◽  
Suguru Honma ◽  
...  
Keyword(s):  
Heart Failure ◽  
Body Fat ◽  
Fat Mass ◽  
Cardiac Event ◽  
Muscle Wasting ◽  
Obesity Paradox ◽  
Percent Body Fat ◽  
Body Fat Mass ◽  
Cardiac Events ◽  
Kaplan Meier

Abstract Background Although high body mass index (BMI) is a risk factor of heart failure (HF), HF patients with a higher BMI had a lower mortality rate than that in HF patients with normal or lower BMI, a phenomenon that has been termed the “obesity paradox”. However, the relationship between body composition, i.e., fat or muscle mass, and clinical outcome in HF remains unclear. Methods We retrospectively analyzed data for 198 consecutive HF patients (76 years of age; males, 49%). Patients who were admitted to our institute for diagnosis and management of HF and received a dual-energy X-ray absorptiometry scan were included regardless of left ventricular ejection fraction (LVEF) categories. Muscle wasting was defined as appendicular skeletal muscle mass index < 7.0 kg/m2 in males and < 5.4 kg/m2 in females. Increased percent body fat mass (increased FM) was defined as percent body fat > 25% in males and > 30% in females. Results The median age of the patients was 76 years (interquartile range [IQR], 67–82 years) and 49% of them were male. The median LVEF was 47% (IQR, 33–63%) and 33% of the patients had heart failure with reduced ejection fraction. Increased FM and muscle wasting were observed in 58 and 67% of the enrolled patients, respectively. During a 180-day follow-up period, 32 patients (16%) had cardiac events defined as cardiac death or readmission by worsening HF or arrhythmia. Kaplan-Meier survival curves showed that patients with increased FM had a lower cardiac event rate than did patients without increased FM (11.4% vs. 22.6%, p = 0.03). Kaplan-Meier curves of cardiac event rates did not differ between patients with and those without muscle wasting (16.5% vs. 15.4%, p = 0.93). In multivariate Cox regression analyses, increased FM was independently associated with lower cardiac event rates (hazard ratio: 0.45, 95% confidence interval: 0.22–0.93) after adjustment for age, sex, diabetes, muscle wasting, and renal function. Conclusions High percent body fat mass is associated with lower risk of short-term cardiac events in HF patients.

Sign in / Sign up

Export Citation Format

Share Document