scholarly journals The relationship between Lipocalin-2 level and hepatic steatosis in obese patients with NAFLD after bariatric surgery

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiaqi Chen ◽  
Shihui Lei ◽  
Yueye Huang ◽  
Xiaojuan Zha ◽  
Lei Gu ◽  
...  

Abstract Background Lipocalin-2 (LCN2) has a critical effect on obesity as well as its associated comorbidities. The present study focused on analyzing serum LCN2 levels of obese patients with nonalcoholic fatty liver disease (NAFLD) and on determining relationship of hepatic steatosis improvement with LCN2 levels after laparoscopic sleeve gastrectomy (LSG). Methods This work enrolled ninety patients with obesity and NAFLD. Twenty-three of them underwent LSG. Anthropometric and biochemical parameters and serum LCN2 levels were determined at baseline and those at 6-month post-LSG. Controlled attenuation parameter (CAP) measured by FibroScan was adopted for evaluating hepatic steatosis. Results Among severe obesity patients, serum LCN2 levels were significantly increased (111.59 ± 51.16 ng/mL vs. 92.68 ± 32.68 ng/mL, P = 0.035). The CAP value was higher indicating higher liver fat content (360.51 ± 45.14 dB/m vs. 340.78 ± 45.02 dB/m, P = 0.044). With regard to surgical patients, liver function, glucose, and lipid levels were significantly improved after surgery. Serum LCN2 levels significantly decreased (119.74 ± 36.15 ng/mL vs. 87.38 ± 51.65 ng/mL, P = 0.001). Decreased CAP indicated a significant decrease in liver fat content (358.48 ± 46.13 dB/m vs. 260.83 ± 69.64 dB/m, P < 0.001). The decrease in LCN2 levels was significantly related to the reduced hepatic fat content and improvement in steatosis grade after adjusting for gender, age, and BMI decrease. Conclusions Serum LCN2 levels are related to obesity and NAFLD. The decreased serum LCN2 levels could be an indicator of hepatic steatosis improvement.

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Hans-Erik Johansson ◽  
Arvo Haenni ◽  
Björn Zethelius

Background. Obesity is characterized by liver steatosis, chronic inflammation, and increased liver enzymes, that is, gamma-glutamyltransferase (GGT) and alanine aminotransferase (ALT), markers for nonalcoholic fatty liver disease (NAFLD) and liver fat content. Increased platelet counts (PCs) are associated with inflammatory conditions and are a valuable biomarker of the degree of fibrosis in NAFLD. We investigated alterations in PC, GGT, and ALT after biliopancreatic diversion with duodenal switch (BPD-DS) and Roux-en-Y gastric bypass (RYGBP).Methods. Ten morbidly obese patients (body mass index, BMI:53.5±3.8 kg/m2) who underwent BPD-DS were evaluated preoperatively (baseline) and 1 year (1st followup) and 3 years (2nd followup) after surgery and compared with 21 morbidly obese patients (BMI:42.3±5.2 kg/m2) who underwent RYGBP.Results. Over the 3 years of followup, changes in BPD-DS and RYGBP patients (BPD-DS/RYGBP) were as follows: BMI (−44%/−24%), GGT (−63%/−52%), and ALT (−48%/−62%). PC decreased (−21%) statistically significantly only in BPD-DS patients.Conclusions. Morbidly obese patients treated by RYGBP or BPD-DS show sustained reductions in BMI, ALT, and GGT. The decrease in PC and liver enzymes after BPD-DS may reflect a more pronounced decrease of liver-fat-content-related inflammation and, as a result, a lowered secondary thrombocytosis.


2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Cristina Galarregui ◽  
M. Angeles Zulet ◽  
Bertha Araceli Marin-Alejandre ◽  
Irene Cantero ◽  
Nora Goodwin ◽  
...  

AbstractIntroductionDietary components are contributing factors in the development of Nonalcoholic fatty liver disease (NAFLD). The glycaemic index (GI), glycaemic load (GL) and total antioxidant capacity (TAC) have been considered potential dietary tools influencing diet–disease relationships. The aim of this study was to evaluate associations of the dietary GI, GL, TAC and insulin resistance (IR) condition with hepatic fat in NAFLD adults.Material and methods: 112 overweight/obese adults with NAFLD (age: 50.8 ± 9 years old) were included in the trial. Dietary intake was assessed by a validated 137-item food frequency questionnaire (FFQ). Anthropometric, glycemic and lipid profiles, fatty liver quantification by magnetic resonance imaging (MRI) and IR measured by the Homeostatic Model Assessment of IR (HOMA-IR) were assessed at baseline. This study was registered as FLiO: Fatty Liver in Obesity study; NCT03183193.Results: The median of liver fat content by MRI was 6.4 (3.8–10.9) in the recruited population. Participants with higher liver fat content showed significantly increased values of glucose, insulin, HbA1c and HOMA-IR than those with lower liver fat content (p < 0.05). Correlation analyses revealed relevant positive associations of hepatic fat with GI (r = 0.17; p = 0.077) and GL (r = 0.19; p = 0.047). Also, a negative association between liver fat content and TAC (r = -0.22; p = 0.023) was found. Linear regression analyses were used to examine the associations of hepatic fat and dietary quality indicators as well as IR adjusted for potential confounders (sex, age and physical activity). The final models showed that HOMA-IR, GI, GL and TAC were able to explain between 22.4 and 22.8 % (p < 0.001) of the variability of liver fat content.DiscussionThe pathophysiology of NAFLD is thought to be associated with dietary determinants that contribute to metabolic dysregulation such as IR, ectopic liver fat deposition and hepatic damage. In accordance with other authors, we suggest that monitoring GI, GL and TAC may be useful approaches for the dietary treatment of NAFLD since they are related to hepatic fat. Additionally, it is important to highlight the essential role of IR in NAFLD as a key mediator in the development of NAFLD. Certainly, findings of the present study revealed a significant association of hepatic fat accumulation and IR.In summary, GI, GL and TAC are potential markers of diet quality, with an impact on susceptible population at hepatic risk.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Kwang Baek Kim ◽  
Chang Won Kim

Accurate measures of liver fat content are essential for investigating hepatic steatosis. For a noninvasive inexpensive ultrasonographic analysis, it is necessary to validate the quantitative assessment of liver fat content so that fully automated reliable computer-aided software can assist medical practitioners without any operator subjectivity. In this study, we attempt to quantify the hepatorenal index difference between the liver and the kidney with respect to the multiple severity status of hepatic steatosis. In order to do this, a series of carefully designed image processing techniques, including fuzzy stretching and edge tracking, are applied to extract regions of interest. Then, an unsupervised neural learning algorithm, the self-organizing map, is designed to establish characteristic clusters from the image, and the distribution of the hepatorenal index values with respect to the different levels of the fatty liver status is experimentally verified to estimate the differences in the distribution of the hepatorenal index. Such findings will be useful in building reliable computer-aided diagnostic software if combined with a good set of other characteristic feature sets and powerful machine learning classifiers in the future.


2014 ◽  
Vol 6 (1) ◽  
pp. 16-24 ◽  
Author(s):  
S. C. McLeay ◽  
G. A. Morrish ◽  
T. K. Ponnuswamy ◽  
B. Devanand ◽  
M. Ramanathan ◽  
...  

The aim of this study was to assess and compare fat content within the liver for normal (body mass index (BMI) < 25 kg/m2), overweight (25-30 kg/m2) and obese (≥ 30 kg/m2) subjects using a noninvasive, non-contrast computed tomography (CT) quantification method. Adult subjects aged 18-60 yrs scheduled to undergo CT examination of the abdominal region were recruited for this study, stratified across BMI categories. Liver volume, fat content, and lean liver volume were determined using CT methods. A total of 100 subjects were recruited, including 30 normal weight, 31 overweight, and 39 obese. Total liver volume increased with BMI, with mean values of 1138 ± 277, 1374 ± 331, and 1766 ± 389 cm3 for the normal, overweight, and obese, respectively (P < 0.001), which was due to an increase in both liver fat content and lean liver volume with BMI. Some obese subjects had no or minimal hepatic fat content. The prevalence of mild fatty liver in this study of 100 subjects was overestimated for all BMI categories using a range of qualitative diagnostic measures, with predicted prevalence of fatty liver in obese subjects ranging from 76.9% for liver-to-spleen ratio ≤ 1.1 to 89.7% for liver attenuation index (liver HU - spleen HU) ≤ 40, compared to 66.7% by quantification of fat content. Results show that total liver volume increases with BMI, however, not all obese subjects display fatty infiltration of the liver. CT quantification of liver fat content may be suitable for accurate diagnosis of hepatic steatosis in clinical practice and assessment of donor livers for transplantation.


2020 ◽  
Vol 22 (1) ◽  
pp. 22-28 ◽  
Author(s):  
Ziba Keymasi ◽  
Abbas Sadeghi ◽  
Hassan Pourrazi

Background and aims: Non-alcoholic fatty liver disease (NAFLD), which is associated with fat accumulation and deposition in liver cells, is a serious risk factor for other diseases such as cardiovascular disorders and diabetes. The aim of this study was to investigate the effect of Pilates training on hepatic fat content and liver enzymes in men with NAFLD in 2019. Methods: In this semi-experimental study, 20 men with NAFLD were randomly divided into Pilates training (n=10) and control (n=10) groups. The Pilates group participated in the Pilates training program for eight weeks (three 60-minute sessions per week), whereas the control group engaged in no regular physical activity. The body composition, anthropometric indices, liver fat content, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured before and after the training period. Eventually, data were analyzed using paired and independent t tests at a significance level of 0.05 by SPSS 18. Results: After eight weeks of Pilates training, liver fat content in the Pilates group was significantly lower than that in the control group (P=0.001). Further, the serum levels of ALT, AST, and ALP significantly decreased in the Pilates group compared to the control group (P=0.04, P=0.05, and P=0.02, respectively). In addition, eight weeks of Pilates training significantly reduced body weight, body mass index (BMI), fat percentage, and the waist-to-hip ratio of patients, while no significant changes were observed in the control group. Conclusion: The results of the present study indicated that Pilates training could be effective in improving liver fat content and reducing the serum levels of ALT, AST, and ALP in men with NAFLD. Furthermore, Pilates training helps to improve body composition and anthropometric indices in patients afflicted with NAFLD and can have a role in the management of this condition.


2019 ◽  
Vol 8 (8) ◽  
pp. 1097-1107 ◽  
Author(s):  
Lena-Maria Levin ◽  
Henry Völzke ◽  
Markus M Lerch ◽  
Jens-Peter Kühn ◽  
Matthias Nauck ◽  
...  

Objective Chemerin and adiponectin are adipokines assumed to be involved in the development of metabolic syndrome-related phenotypes like hepatic steatosis. We aimed to evaluate the associations of circulating chemerin and adiponectin concentrations with liver enzymes, liver fat content, and hepatic steatosis in the general population. Methods Data of 3951 subjects from the population-based Study of Health in Pomerania (SHIP-TREND) were used. Hepatic steatosis was assumed when either a hyperechogenic liver (assessed via ultrasound) or a magnetic resonance imaging (MRI)-quantified liver fat content >5% was present. Adjusted sex-specific quantile and logistic regression models were applied to analyze the associations of chemerin and adiponectin with liver enzymes, liver fat content and hepatic steatosis. Results The observed associations of chemerin and adiponectin with liver enzymes were very divergent depending on sex, fasting status and the specific enzyme. More consistent results were seen in the analyses of these adipokines in relation to MRI-quantified liver fat content. Here, we observed inverse associations to adiponectin in both sexes as well as a positive (men) or U-shaped (women) association to chemerin. Similarly, the MRI-based definition of hepatic steatosis revealed strongly consistent results: in both sexes, high chemerin concentrations were associated with higher odds of hepatic steatosis, whereas high adiponectin concentrations were associated with lower odds. Conclusion Our results suggest a role of these adipokines in the pathogenesis of hepatic steatosis independent of metabolic or inflammatory disorders. However, experimental studies are needed to further clarify the underlying mechanisms and the inter-play between adipokine concentrations and hepatic steatosis.


Author(s):  
Xiaoming Ma ◽  
Xing Xue ◽  
Jingxin Zhang ◽  
Shuang Liang ◽  
Chunfang Xu ◽  
...  

Abstract Background and Aims Liver expressed antimicrobial peptide 2 (LEAP2) is recently identified as a regulator in energy metabolism. This study aims to 1) investigate the role of leap2 in hepatic steatosis in C57BL/6 mice; 2) evaluate the association between circulating LEAP2 levels and liver fat contents in a hospital based case-control study. Methods The rodent experiment: western blotting and qPCR were performed to evaluate leap2 levels, lipid metabolism pathways and insulin signaling. shRNA was used to knockdown leap2. The clinical study: commercial ELISA kits were used to measure circulating LEAP2 levels (validated by western blotting). Liver fat content was estimated using MRI-derived proton density fat fraction and FibroScan-derived controlled attenuation parameter. Results The rodent experiment found the hepatic expression and secreted levels of leap2 were increased in mice with diet-induced steatosis. Leap2 knockdown ameliorated steatosis via lipolytic/lipogenic pathway and improved insulin sensitivity via IRS/AKT signaling. The clinical study reported increased circulating levels of LEAP2 in the subjects with steatosis. Moreover, LEAP2 correlated positively with age, body mass index, waist-to-hip ratio, liver fat content, fasting insulin and HOMA-IR, whereas inversely with acyl-ghrelin. Furthermore, the circulating levels of LEAP2 are dependent on liver fat content, acyl-ghrelin and fasting glucose. Lastly, circulating LEAP2 is an independent predictor of NAFLD. Conclusions The study suggests LEAP2 is associated with hepatic steatosis, which may involve lipolytic/lipogenic pathway and insulin signaling.


2014 ◽  
Vol 171 (5) ◽  
pp. 561-569 ◽  
Author(s):  
Daniel J Cuthbertson ◽  
Martin O Weickert ◽  
Daniel Lythgoe ◽  
Victoria S Sprung ◽  
Rebecca Dobson ◽  
...  

Background and aimsSimple clinical algorithms including the fatty liver index (FLI) and lipid accumulation product (LAP) have been developed as surrogate markers for non-alcoholic fatty liver disease (NAFLD), constructed using (semi-quantitative) ultrasonography. This study aimed to validate FLI and LAP as measures of hepatic steatosis, as determined quantitatively by proton magnetic resonance spectroscopy (1H-MRS).MethodsData were collected from 168 patients with NAFLD and 168 controls who had undergone clinical, biochemical and anthropometric assessment. Values of FLI and LAP were determined and assessed both as predictors of the presence of hepatic steatosis (liver fat >5.5%) and of actual liver fat content, as measured by 1H-MRS. The discriminative ability of FLI and LAP was estimated using the area under the receiver operator characteristic curve (AUROC). As FLI can also be interpreted as a predictive probability of hepatic steatosis, we assessed how well calibrated it was in our cohort. Linear regression with prediction intervals was used to assess the ability of FLI and LAP to predict liver fat content. Further validation was provided in 54 patients with type 2 diabetes mellitus.ResultsFLI, LAP and alanine transferase discriminated between patients with and without steatosis with an AUROC of 0.79 (IQR=0.74, 0.84), 0.78 (IQR=0.72, 0.83) and 0.83 (IQR=0.79, 0.88) respectively although could not quantitatively predict liver fat. Additionally, the algorithms accurately matched the observed percentages of patients with hepatic steatosis in our cohort.ConclusionsFLI and LAP may be used to identify patients with hepatic steatosis clinically or for research purposes but could not predict liver fat content.


2015 ◽  
Vol 100 (5) ◽  
pp. E821-E825 ◽  
Author(s):  
Rosellina M. Mancina ◽  
Niina Matikainen ◽  
Cristina Maglio ◽  
Sanni Söderlund ◽  
Nina Lundbom ◽  
...  

Abstract Context: Nonalcoholic fatty liver disease (NAFLD) is an emerging epidemic disease characterized by increased hepatic fat, due to an imbalance between synthesis and removal of hepatic lipids. In particular, increased hepatic de novo lipogenesis (DNL) is a key feature associated with NAFLD. The genetic variations I148M in PNPLA3 and E167K in TM6SF2 confer susceptibility to NAFLD. Objective: Here we aimed to investigate the contribution of DNL to liver fat accumulation in the PNPLA3 I148M or TM6SF2 E167K genetic determinants of NAFLD. Patients and Methods: The PNPLA3 I148M and TM6SF2 E167K were genotyped in two well-characterized cohorts of Europeans. In the first cohort (Helsinki cohort; n = 88), we directly quantified hepatic DNL using deuterated water. In the second cohort (Milan cohort; n = 63), we quantified the hepatic expression of SREBP1c that we have found previously associated with increased fat content. Liver fat was measured by magnetic resonance proton spectroscopy in the Helsinki cohort, and by histological assessment of liver biopsies in the Milan cohort. Results: PNPLA3 148M was associated with lower DNL and expression of the lipogenic transcription factor SREBP1c despite substantial increased hepatic fat content. Conclusions: Our data show a paradoxical dissociation between hepatic DNL and hepatic fat content due to the PNPLA3 148M allele indicating that increased DNL is not a key feature in all individuals with hepatic steatosis, and reinforces the contribution of decreased mobilization of hepatic triglycerides for hepatic lipid accumulation in subject with the PNPLA3 148M allele.


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