Acid Lipase Activity Research Articles

Lysosomal acid lipase activity in children with dyslipidemia and hepatic dysfunction

Lysosomal acid lipase activity in children with dyslipidemia and hepatic dysfunction

Lipid accumulation impairs lysosomal acid lipase activity in hepatocytes: Evidence in NAFLD patients and cell cultures

AimsIt has been hypothesized that the activity of lysosomal acid lipase (LAL), a key enzyme involved in lipid metabolism, is involved in the NAFLD phenotype. To clarify the role of LAL in NAFLD, we studied 164 consecutive patients with biopsy-proven NAFLD and fat-loaded HepG2 cells. MethodsLAL activity was measured (i) on dried blood spots (DBS) from NAFLD patients and dyslipidemic subjects without fatty liver and (ii) on liver biopsies from NAFLD patients. LAL activity and expression were evaluated in HepG2 cells cultured in the presence of free fatty acids (FAs), with or without a PPAR-alpha agonist. ResultsLAL activity was significantly reduced in patients with NAFLD compared to dyslipidemic subjects. LAL activity measured in liver biopsies from NAFLD patients was highly correlated to that measured on DBS and was independent of LAL expression in the liver. In a fully adjusted model, LAL activity on DBS was associated only with platelets and, when normalized by platelet count, it did not differ according to fibrosis stage. In vitro, FA loading of HepG2 fully replicated the impairment of LAL activity observed in NALFD patients. In these cells, the activation of PPAR-alpha receptors prevented and corrected FA-induced LAL impairment, by stimulating FA oxidation and LAL expression. ConclusionsLAL activity is reduced in NAFLD patients, independently from disease progression. In vitro, impaired LAL activity induced by FA loading was rescued by PPAR-alpha activation. These data suggest that the pharmacological modulation of LAL should be explored in the management of NAFLD patients.

Lysosomal acid lipase activity and liver fibrosis in the clinical continuum of non-alcoholic fatty liver disease.

Recent evidence showed a reduced activity of the lysosomal acid lipase (LAL) in patients with non-alcoholic fatty liver disease (NAFLD) and cryptogenic cirrhosis (CC). However, the relationship between LAL activity and liver fibrosis has never been investigated. Cross-sectional study including 575 outpatients referred for the management of cardio-metabolic and liver disease. The absence of liver fibrosis was defined by a FIB-4<1.30 and NAFLD fibrosis score (NFS) <-1.455. LAL activity was measured with dried blood spot technique. Overall, 515 patients had a diagnosis of NAFLD (454 NAFL and 61 biopsy-proven NASH) and 60 of CC. The value of LAL activity progressively decreased from healthy subjects to NAFL/NASH patients to CC (P<.001). LAL activity was reduced by 10% in patients with NAFL, by 20% in NASH and by 50% in CC. The prevalence of CC decreased across the tertiles of LAL activity: 22.2% in the lowest, 4.6% in the intermediate and 0.5% in the highest tertile. In NAFLD patients, 69.9% had a FIB4<1.30, and 43.1% a NFS <-1.455. Multivariate logistic regression analysis showed that Log(LAL activity) was associated with FIB-4<1.30 (Odds ratio [OR] 2.19 95% confidence interval [CI] 1.33-3.62, P=.002) and NFS < -1.455 (OR 2.43, 95% CI 1.51-3.91, P<.001) after adjustment for confounding factors. We found a progressive reduction of LAL activity according to liver disease severity. LAL activity was inversely associated with markers of liver fibrosis in patients with NAFLD.

Reduced lysosomal acid lipase activity: A new marker of liver disease severity across the clinical continuum of non-alcoholic fatty liver disease?

Lysosomal acid lipase (LAL) plays a key role in intracellular lipid metabolism. Reduced LAL activity promotes increased multi-organ lysosomal cholesterol ester storage, as observed in two recessive autosomal genetic diseases, Wolman disease and Cholesterol ester storage disease. Severe liver steatosis and accelerated liver fibrosis are common features in patients with genetic LAL deficiency. By contrast, few reliable data are available on the modulation of LAL activity in vivo and on the epigenetic and metabolic factors capable of regulating its activity in subjects without homozygous mutations of the Lipase A gene. In the last few years, a less severe and non-genetic reduction of LAL activity was reported in children and adults with non-alcoholic fatty liver disease (NAFLD), suggesting a possible role of LAL reduction in the pathogenesis and progression of the disease. Patients with NAFLD show a significant, progressive reduction of LAL activity from simple steatosis to non-alcoholic steatohepatitis and cryptogenic cirrhosis. Among cirrhosis of different etiologies, those with cryptogenic cirrhosis show the most significant reductions of LAL activity. These findings suggest that the modulation of LAL activity may become a possible new therapeutic target for patients with more advanced forms of NAFLD. Moreover, the measurement of LAL activity may represent a possible new marker of disease severity in this clinical setting.

Changes in Lipase and Antioxidant Enzyme Activities during Processing of Cantonese Sausage with D-Sodium Erythorbate

Pork was used as raw material to produce Cantonese sausage, with additions of 0.05% or 0.1% D-sodium erythorbate. The oxidation indices (peroxide value, TBARS value, carbonyl value, and conjugated dienes value) and enzyme activity (total phospholipase, acid lipase, neutral lipase, superoxide dismutase, and glutathione peroxidase) were measured in the sausages at different processing periods. The results showed slowed lipid oxidation in the presence of D-sodium erythorbate, inhibition of total phospholipase, acid lipase, and neutral lipase activities, and increased superoxide dismutase activity, with little change in glutathione peroxidase activities. When increasing D-sodium erythorbate, the superoxide dismutase activity was negatively correlated with the peroxide value at 5 h (P&lt;0.01), the neutral lipase activity was positively correlated with the conjugated dienes value at 15 h (P&lt;0.01), and the total phospholipase activity was positively correlated with the peroxide value at 30 h (P&lt;0.01). This study explored the antioxidant effect of D-sodium erythorbate and provides a theoretical foundation to improve the quality of Cantonese sausage.

Lysosomal Acid Lipase as a Molecular Target of the Very Low Carbohydrate Ketogenic Diet in Morbidly Obese Patients: The Potential Effects on Liver Steatosis and Cardiovascular Risk Factors.

A very low carbohydrate ketogenic diet (VLCKD) is an emerging technique to induce a significant, well-tolerated, and rapid loss of body weight in morbidly obese patients. The low activity of lysosomal acid lipase (LAL) could be involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), which is a common feature in morbidly obese patients. Fifty-two obese patients suitable for a bariatric surgery intervention underwent a 25-day-long VLCKD. The biochemical markers of glucose and lipid metabolism, and flow-mediated dilation (FMD) of the brachial artery were measured before and after VLCKD. LAL activity was measured using the dried blood spot technique in 20 obese patients and in a control group of 20 healthy, normal-weight subjects. After VLCKD, we observed a significant reduction in body mass index, fasting glucose, insulinemia, and lipid profile parameters. No significant variation in FMD was observed. The number of patients with severe liver steatosis significantly decreased. LAL activity significantly increased, although the levels were not significantly different as compared to the control group. In conclusion, VLCKD induces the activity of LAL in morbidly obese subjects and reduces the secretion of all circulating lipoproteins. These effects could be attributed to the peculiar composition of the diet, which is particularly poor in carbohydrates and relatively rich in proteins.

Opening a window on lysosomal acid lipase deficiency: Biochemical, molecular, and epidemiological insights.

Lysosomal acid lipase deficiency (LAL-D) is a multi-organ autosomal recessive disease caused by mutations in LIPA. We reviewed data from 681 samples (white blood cells [WBC] n = 625, fibroblasts = 30, liver = 4, amniocytes = 13, chorionic villus = 9) received for analysis of lysosomal acid lipase (LAL) activity over a 15-year period. LIPA sequencing was performed in 49 patients with reduced (n = 26) or deficient (n = 23) LAL activity. The Exome Aggregation Consortium and Genome Aggregation Database dataset were used for LAL-D prevalence calculations. LAL WBC activity was reduced in 67 patients (10.72%) and deficient in 37 (5.92%). The average of LAL activity ± margin of error (CI 95%) was 19.32 ± 0.86 pmol/min/mg for reduced activity patients and 5.90 ± 1.42 pmol/min/mg for deficient patients. The average age at diagnosis for LAL-D was 23.6 years with several patients older than age 30. The correlation between the age at diagnosis and LAL activity showed a significant moderate direct correlation (Pearson's r = 0.46, P < 0.005). Homozygous or compound heterozygous mutations were identified in 9 out of 23 patients with deficient results (detection rate 39.1%). The average LAL activity in molecularly confirmed patients was 4.02 ± 2.02 pmol/min/mg protein, while in molecularly negative patients was 13.886 ± 1.49 pmol/min/mg (P < 0.0001). Twenty-two different mutations were identified including two novel variants (c.309C>A and c.856G>C). A carrier frequency of approximately 1 in 350 was inferred. LAL activity in WBC is a validated tool for LAL-D diagnosis. Higher residual enzymatic activity might result in a milder phenotype leading to diagnosis delay. A cut-off below 12 pmol/min/mg protein might be useful to discriminate patients with LIPA mutations.

Lysosomal Acid Lipase: Can it be a New Non-Invasive Serum Biomarker of Cryptogenic Liver Fibrosis and Cirrhosis?

Introduction and aim. The association between lysosomal acid lipase (LAL) activity and liver steatosis or fibrosis is poorly studied. The aim of our study was to determine the predictive power of LAL for cryptogenic liver steatosis and cryptogenic significant fibrosis/cirrhosis.Material and methods. Cross-sectional observational study of 101 adult patients with unexplained elevated liver enzymes/hepatomegaly with or without dyslipidemia submitted to the determination of LAL activity and LIPA gene (E8SJM-C.894G^A) mutation. Seventy-one patients underwent liver biopsy or FibroScan®. Patients with an identifiable liver dysfunction cause and well-stablished NAFLD/NASH risk factors were excluded. Predictors for liver steatosis, significant fibrosis (> F2) or cirrhosis (F4) were evaluated.Results. Liver steatosis and fibrosis were mainly assessed by liver biopsy (74.6%; n = 53). Steatosis was present in 62.0% (n = 44), significant fibrosis in 47.9% (n = 34) and cirrhosis in 39.4% (n = 28). The median LAL was 0.36 (0.21-0.46)nmol/spot/h (vs. 0.29 (0.20-0.47); p = 0.558) for liver steatosis, 0.22 (0.11-0.29) nmol/spot/h (vs. 0.40 (0.34-0.51); p <0.001) for significant fibrosis and 0.21 (0.11-0.27) nmol/spot/h (vs. 0.40 (0.32-0.52); p < 0.001) for cirrhosis. No LIPA gene mutations were found. LAL activity was the strongest predictor of significant fibrosis (AUROC: 0.833; p < 0.001) with a cut-off of 0.265 (sensitivity: 85.9%; specificity: 75.0%) and cirrhosis (AUROC: 0.859; p < 0.001) with a cut-off of 0.235 (sensitivity: 86.2%; specificity: 75.0%), being higher than FIB4, GUCI or APRI. However, LAL activity was not associated with liver steatosis (AUROC: 0.536; p =0.558).Conclusion. LAL activity can be considered a non-invasive new marker of cryptogenic liver fibrosis with higher accuracy than other known biomarkers. LAL activity < 0.265 nmol/spot/h was strongly associated with cryptogenic significant fibrosis and <0.235 nmol/spot/h with cryptogenic cirrhosis. LAL activity was not associated with cryptogenic liver steatosis.

Lysosomal Acid Lipase Deficiency: An Uncommon Masquerader

Lysosomal acid lipase deficiency (LALD) is a rare genetic disorder. This disease is due to decreased activity of lysosomal acid lipase which results in accumulation of cholesterol esters in lysosomes. This leads to liver cell damage and ultimately hepatic fibrosis. Most LALD patients present with abnormal liver enzymes and hyperlipidemia (HLD). In addition, patients with LALD have microvesicular steatosis on liver biopsy. However, this disease's presentation is not unique. The patient is a 29 year old male presenting with HLD and elevated liver enzymes. His workup was only significant for an anti-nuclear antibody titer of 1:160. Viral hepatitis serologies, ceruloplasmin, alpha-1 antitrypsin and iron studies were all within normal limits. A liver biopsy revealed diffuse microvesicular and medium droplet steatosis without large droplet fat vacuoles. Trichrome and reticulin stains showed thin bridging fibrosis (see image 1). Non-alcoholic steatohepatitis (NASH) was the presumptive diagnosis. His liver enzymes remained persistently elevated even after significant lifestyle modification and his lysosomal acid lipase level was tested. His enzyme level was undetectable and he was started on enzyme replacement therapy with sebelipase alfa. This case describes a common presentation of a rare disease, LALD. Due to the low incidence and nonspecific laboratory presentation of this disease, LALD is often misdiagnosed. NASH is becoming increasingly prevalent and is commonly diagnosed in patients with HLD and abnormal liver enzymes. A liver biopsy in a patient with this presentation that shows microvesicular steatosis will point the differential towards NASH. In those with NASH, statins are a mainstay therapy, but there is little evidence that these medications have benefit in LALD. While statins improve LDL and cholesterol levels in those with LALD, there is usually continued progression of liver disease with worsening steatosis and fibrosis. Therefore LALD patients misdiagnosed with NASH will receive incomplete therapy. The enzyme replacement agent sebelipase alfa hydrolyzes cholesterol esters that build up to cause the liver damage associated with LALD. Clinical trials with this drug have shown statistically significant decreases in LDL and liver enzymes in those with LALD. Now that there are treatment strategies for LALD, keeping this disease in the differential in patients with elevated liver enzymes and HLD is vital to ensure a chance at proper treatment.2325 Figure 1. Panel A: Medium drop-let macrovesicular steatosis and microvesicular steatosis Panel B: Acidophilic body Panel C: Kupffer cells with fat droplets Panel D: Bridging fibrosis

Lysosomal acid lipase activity is reduced in NAFLD: Mechanisms and rescue by PPAR-alpha agonists

Lysosomal acid lipase activity is reduced in NAFLD: Mechanisms and rescue by PPAR-alpha agonists

Lysosomal Acid Lipase: Can it be a New Non-Invasive Serum Biomarker of Cryptogenic Liver Fibrosis and Cirrhosis?

Introduction and aim. The association between lysosomal acid lipase (LAL) activity and liver steatosis or fibrosis is poorly studied. The aim of our study was to determine the predictive power of LAL for cryptogenic liver steatosis and cryptogenic significant fibrosis/ cirrhosis. Material and methods. Cross-sectional observational study of 101 adult patients with unexplained elevated liver enzymes/hepatomegaly with or without dyslipidemia submitted to the determination of LAL activity and LIPA gene (E8SJMC. 894G→A) mutation. Seventy-one patients underwent liver biopsy or FibroScan®. Patients with an identifiable liver dysfunction cause and well-stablished NAFLD/NASH risk factors were excluded. Predictors for liver steatosis, significant fibrosis (≥ F2) or cirrosis (F4) were evaluated. Results. Liver steatosis and fibrosis were mainly assessed by liver biopsy (74.6%; n = 53). Steatosis was present in 62.0% (n = 44), significant fibrosis in 47.9% (n = 34) and cirrhosis in 39.4% (n = 28). The median LAL was 0.36 (0.21-0.46)nmol/spot/h (vs. 0.29 (0.20-0.47); p = 0.558) for liver steatosis, 0.22 (0.11-0.29) nmol/spot/h (vs. 0.40 (0.34-0.51); p &lt; 0.001) for significant fibrosis and 0.21 (0.11-0.27) nmol/spot/h (vs. 0.40 (0.32-0.52); p &lt; 0.001) for cirrhosis. No LIPA gene mutations were found. LAL activity was the strongest predictor of significant fibrosis (AUROC: 0.833; p &lt; 0.001) with a cut-off of 0.265 (sensitivity: 85.9%; specificity: 75.0%) and cirrhosis (AUROC: 0.859; p &lt; 0.001) with a cut-off of 0.235 (sensitivity: 86.2%; specificity: 75.0%), being higher than FIB4, GUCI or APRI. However, LAL activity was not associated with liver steatosis (AUROC: 0.536; p = 0.558). Conclusion. LAL activity can be considered a non-invasive new marker of cryptogenic liver fibrosis with higher accuracy than other known biomarkers. LAL activity &lt; 0.265 nmol/spot/h was strongly associated with cryptogenic significant fibrosis and &lt; 0.235 nmol/spot/h with cryptogenic cirrhosis. LAL activity was not associated with cryptogenic liver steatosis.

Cholesteryl Ester Storage Disease – A Rare Presentation

Cholesteryl Ester Storage Disease (CESD) is a rare genetic disease characterized by accumulation of cholesteryl esters and triglycerides in many tissues due to deficiency of Lysosomal Acid Lipase (LAL/ LIPA) enzyme, which is essential for hydrolysis of triglycerides and cholesterol esters in lysosomes.1 The diagnosis is indicated by abnormal lipid profile, deposition of cholesterol crystals in internal organs and reduced acid lipase activity in leukocytes. Here we report a 16 year-old girl who presented with repeated episodes of hepatic encephalopathy with onset of first symptom at 9 years of age with history of consanguinity of marriage between parents. On examination, we found hepatosplenomegaly. Laboratory examination showed abnormal lipid profile and reduced activity of acid lipase enzyme in leukocytes. After exclusion of other possible pathological conditions and on the basis of lab criteria, we diagnose the case as Cholesteryl Ester Storage Disease (CESD).J MEDICINE JUL 2018; 19 (2) : 130-132

Lysosomal Acid Lipase Activity Deficiency in Children with Liver Disease:a potential biomarker?

Lysosomal Acid Lipase Activity Deficiency in Children with Liver Disease:a potential biomarker?

Effects of high pressure treatment on lipolysis-oxidation and volatiles of marinated pork meat in soy sauce

To investigate the effect of high pressure (HP) treatment (150 and 300 MPa for 15 min at 20 °C) on lipolysis-oxidation and volatile profile of marinated pork meat in soy sauce, the changes of lipase, phospholipase and lipoxygenase (LOX) activities, TBARS, free fatty acids and volatiles composition in control and HP treated samples were analyzed. Acid and neutral lipase activities and free fatty acids content decreased, while LOX activity and TBARS increased after HP treatment. Phospholipase had well stability under HP. The levels of volatile compounds from lipid oxidation and brine increased under HP and then contributed 73.16–78.25% of the typical aroma, while volatile compounds from carbohydrate fermentation, especially acetic acid, decreased with the pressure increasing. The decrease of free fatty acids during pressurization was probably attributed to the decline of lipase activity and the increase of LOX activity. These findings indicated that HP (150–300 MPa/15 min) promoted lipid oxidation and the permeation of brine, but inhibited carbohydrate fermentation.

Effect of gamma irradiation on the physicochemical properties and nutrient contents of peanut

This study aims to assess the effect of gamma irradiation on the physicochemical properties and nutrient contents of two different peanut cultivars. The peanuts were treated with 0, 1, 3, 5, and 10 kGy gamma irradiation doses. The examined physicochemical properties were water activity, fatty acid value (FAV), peroxide value (PV), carbonyl value (CV), malondialdehyde (MDA) content, and lipase activity. The examined nutrient contents were moisture and ash contents, total sugar, protein and fat contents, fatty acid and amino acid composition. Results showed that high irradiation dose (10 kGy) significantly decreased the fat and protein contents and increased the water activity of peanut. However, the moisture and ash contents and total sugar were not affected by irradiation. The FAV, PV, CV, and MDA contents increased depending on the radiation dose. Fatty acid and amino acid composition changed when the irradiation dose increased. Sodium dodecyl sulfate polyacrylamide gel electrophoresis analysis revealed that irradiation did not modify the protein subunits but disrupted the disulfide bonds. Furthermore, lipase activity decreased with the increased irradiation dose. This phenomenon may positively affect peanut quality during storage.

Response of digestive enzymes and esterases of ecotoxicological concern in earthworms exposed to chlorpyrifos-treated soils.

Assessment of organophosphorus (OP) pesticide exposure in non-target organisms rarely involves non-neural molecular targets. Here we performed a 30-d microcosm experiment with Lumbricus terrestris to determine whether the activity of digestive enzymes (phosphatase, β-glucosidase, carboxylesterase and lipase) was sensitive to chlorpyrifos (5 mg kg-1 wet soil). Likewise, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities were measured in the wall muscle and gastrointestinal tissues as indicators of OP exposure. Chlorpyrifos inhibited the acid phosphatase (34% of controls), carboxylesterase (25.6%) and lipase activities (31%) in the gastrointestinal content. However, in the gastrointestinal tissue, only the carboxylesterase and lipase activities were significantly depressed (42-67% carboxylesterase inhibition in the foregut and crop/gizzard, and 15% lipase inhibition in the foregut). Chlorpyrifos inhibited the activity of both cholinesterases in the gastrointestinal tissues, whereas the AChE activity was affected in the wall muscle. These results suggested chlorpyrifos was widely distributed throughout the earthworm body after 30 d of incubation. Interestingly, we found muscle carboxylesterase activity strongly inhibited (92% of control) compared with that detected in the gastrointestinal tissues of the same OP-exposed individuals. This finding was explained by the occurrence of pesticide-resistant esterases in the gastrointestinal tissues, which were evidenced by zymography. Our results suggest that digestive processes of L. terrestris may be altered by chlorpyrifos, as a consequence of the inhibitory action of the insecticide on some digestive enzymes.

Lipid Degradation During Salt‐Fermented Antarctic Krill Paste Processing and Their Relationship With Lipase and Phospholipase Activities

In this study, lipid degradation during the processing of salt‐fermented Antarctic krill paste is studied by evaluating changes in physicochemical parameters, lipid content, and fatty acid composition, phospholipase (phospholipase A1 [PLA1], phospholipase A2 [PLA2], phospholipase C [PLC], and phospholipase D [PLD]) and lipase activities. Triacylglycerols (TAGs) are an important source of free fatty acids (FFAs) in Antarctic krill paste, causing an increase in FFA content in the early stage of processing, while phospholipids are intensely hydrolyzed during the mid‐late stages. Lipase activities remains constant, while PLA2 and PLD activities increases during all stages of processing. The relative activities of PLA2 and PLC highly correlates with a decline in phosphatidylcholine (PC) and an increase in lysophosphatidylcholine (LPC). A high correlation is also observed between relative PLD activity and increased phosphatidic acid (PA). These results suggest that lipase, PLA2, and PLD contribute to the degradation of lipids during the processing of salt‐fermented Antarctic krill paste.Practical Applications: Due to their abundance of Antarctic krill, fermentation technology can be applied to transform them into a popular condiment. The present study aimes to investigate changes in lipid composition throughout krill salt‐fermentation, and to evaluate their potential effects on fermented krill product. Knowledge of lipase activities during processing is essential to improve the quality of the end products and to further elucidate the complicated mechanisms of lipid degradation.The study of lipid degradation during processing and storage of krill products is of great concern in order to obtain products of high quality and health. Lipid degradation during the processing of salt‐fermented Antarctic krill paste is studied by evaluating changes in physicochemical parameters, lipid content, and fatty acid composition, phospholipase and lipase activities and the study provides information that Lipase, PLA2, and PLD contribute to the degradation of lipids during the processing of salt‐fermented Antarctic krill paste.

Progressive reduction of blood lysosomal acid lipase activity according to stage of adult chronic liver disease and altered enzymatic cellular distribution in cirrhosis

Progressive reduction of blood lysosomal acid lipase activity according to stage of adult chronic liver disease and altered enzymatic cellular distribution in cirrhosis

Effect of aerobic exercise and corn peptide on fat metabolism of overweighed and obese female college students

Objective: This research is aimed to explore the effect of aerobic exercise and corn peptide on fat metabolism of overweighed and obese female college students. Methods: 30 female college students were selected and randomly divided into two groups. Both groups received aerobic exercise. On this basis, the corn peptide group was given corn peptide while the control group was given the same quantity of protein powder. After the experiment, the change of BMI, lipase, and plasma free fatty acid of both groups were compared. Results: The BMI, body mass, and body fat rate of the corn peptide group were lower than the control group. The difference was statistically significant (P<0.05). The plasma free fat acid level and lipase activity of the corn peptide group were significantly higher than the control group. The difference was statistically significant (P<0.05). After experiment, the TC, TG, LDL, and HDL of the corn peptide group were improved. The difference was statistically significant (P<0.05). Conclusion: Corn peptide combined with aerobic exercise (for 8 weeks) can effectively improve the body fat rate and BMI among overweighed and obese female college students.

Activities of Endogenous Lipase and Lipolysis Oxidation of Low-Salt Lactic Acid-Fermented Fish (&lt;i&gt;Decapterus maruadsi&lt;/i&gt;)

There is increasing demand for low-salt meat products that retain traditional flavors. In this study, dry-salted fish (Decapterus maruadsi) were processed by 2 methods to obtain traditional salted fish (HS) and low-salt lactic acid-fermented fish (LAF). The relationship between lipolysis and lipid oxidation was investigated by evaluating changes in endogenous lipase (lipolytic enzymes; lipoxygenase, LOX), free fatty acid composition, thiobarbituric acid reactive substances (TBARS), and peroxide value (POV) during processing. Lipolytic enzyme activity showed a decreasing trend, in general. LOX activity initially increased and eventually decreased. Phospholipase, acid lipase, and neutral lipase activity was 0.33, 0.17, 0.57 (in HS) and 0.39, 0.25, 0.67 (in LAF) times in the final product than the activity levels observed in fresh fish. A principal component analysis indicated that phospholipase and neutral lipase play major roles in promoting lipid hydrolysis (in HS and LAF), the correlation between lipolytic activity and lipid oxidation in HS is greater than the correlation in LAF, and the contribution of LOX to lipid oxidation was minor in salted fish.