Palmitoleic acid is elevated in fatty liver disease and reflects hepatic lipogenesis

Lee, Joseph; Lambert, Jessica E.; Hovhannisyan, Yelena; Ramos-Román, María A.; Trombold, Justin R.; Wagner, David; Parks, Elizabeth J.

doi:10.3945/ajcn.114.092262

Cited by 137 publications

(143 citation statements)

References 62 publications

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“…Plasma (% total FA) PM +ly associated to MetS [65] Overweight adults (n = 24), elevated de novo lipogenesis and liver fat (VLDL)-triacylglycerols (mol% total FA) PM +ly associated with de novo lipogenesis, liver fat, and insulin resistance [63] Women's Health Initiative Memory Study (n = 6379), 11 years followup (n = 703), type-2 diabetes RBC membrane (% total FA) PM +ly associated with type-2 diabetes [64] Men and women (n = 358), aged 30-65 at coronary artery disease risk NEFA (μmol L −1 ) P M +ly association with NAFLD but not with atherosclerosis PM, palmitoleic acid; FFA, free fatty acids; TG, triacylglycerol; RBC, red blood cells; MetS, metabolic syndrome; CHD, coronary heart disease; NAFLD, nonalcoholic fatty liver disease, NASH, non-alcoholic steatohepatitis.…”

Section: Referencementioning

confidence: 99%

“…High levels of plasma palmitoleic acid have been described as a marker of MetS and liver fat accumulation [64,65,84,85] (Table 3). Puri et al [85] observed that plasma palmitoleic acid levels in patients with liver disease increased according to the grade of damage, with higher levels in patients with nonalcoholic steatohepatitis than in those with NAFLD [85] (Table 3).…”

Section: Nafldmentioning

confidence: 99%

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Is Palmitoleic Acid a Plausible Nonpharmacological Strategy to Prevent or Control Chronic Metabolic and Inflammatory Disorders?

Souza

Vannice²,

Neto

et al. 2017

Molecular Nutrition Food Res

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Although dietary fatty acids can modulate metabolic and immune responses, the effects of palmitoleic acid (16:1n-7) remain unclear. Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by β cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. However, human studies report elevated blood levels of palmitoleic acid in people with obesity and metabolic syndrome. These findings might be reflection of the level or activity of stearoyl-CoA desaturase-1, which synthesizes palmitoleate and is enhanced in liver and adipose tissue of obese patients. The aim of this review is to describe the immune-metabolic effects of palmitoleic acid observed in cell culture, animal models, and humans to answer the question of whether palmitoleic acid is a plausible nonpharmacological strategy to prevent, control, or ameliorate chronic metabolic and inflammatory disorders. Despite the beneficial effects observed in cell culture and in animal studies, there are insufficient human intervention studies to fully understand the physiological effects of palmitoleic acid. Therefore, more human-based research is needed to identify whether palmitoleic acid meets the promising therapeutic potential suggested by the preclinical research.

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Section: Referencementioning

confidence: 99%

Section: Nafldmentioning

confidence: 99%

Is Palmitoleic Acid a Plausible Nonpharmacological Strategy to Prevent or Control Chronic Metabolic and Inflammatory Disorders?

Souza

Vannice²,

Neto

et al. 2017

Molecular Nutrition Food Res

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“…Previous studies also indicate that visfatin has an important enzymatic role in De Novo Lipogenesis (DNL) (11,27), which is known to be increased in NAFLD (29,30), yet hepatic and adipose tissue DNL have opposing effects on the prognosis of NAFLD. Hepatic DNL is positively correlated yet adipose tissue DNL is negatively correlated with fatty liver (31,32).…”

Section: Discussionmentioning

confidence: 99%

Interpretation of Serum Visfatin Level in Relation to Hepatic Injury is Probably Gender Dependent in Nonalcoholic Fatty Liver Disease

et al. 2017

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Background: Studies on the association between visfatin and nonalcoholic fatty liver disease (NAFLD) have contradictory results and the role of this adipokine in NAFLD pathogenesis has remained unclear. In vitro studies indicate that visfatin expression could be regulated by sex hormones. Testosterone down-regulates visfatin expression in pre-adipocytes and estrogen increases its expression in adipocytes. Objectives: This study aimed at exploring whether the association between serum visfatin and markers of hepatic injury is the same for both genders in patients with NAFLD. Methods: In this cross-sectional study, 62 consecutive patients (32 males and 30 females) with NAFLD were recruited. Fasting serum visfatin, caspase-cleaved cytokeratin 18 (cCK18), total soluble cytokeratin 18 (CK18), liver enzymes (AST and ALT), insulin, and lipidglucose profile was measured. Anthropometric measurements, fibroscan and assessment of dietary intake and physical activity level, were performed for each participant. Two independent sample t tests, chi-square test, univariate, and multiple linear regression (to adjust for confounding factors) were used to analyze the data. Results: In males, serum visfatin had a significant positive association with serum Aspartate Aminotransferase (AST) (B = 0.47, P = 0.009), alanine aminotransferase (ALT) (B = 0.40, P = 0.035), CK18 (B = 0.50, P = 0.008), and cCK18 (B = 0.47, P = 0.012). In females, serum visfatin only had a weak association with CK18 (B = 0.37, P = 0.045). Instead, higher body mass index (BMI) was significantly associated with increased serum CK18 (B = 0.44, P = 0.02), cCK18 (B = 0.42, P = 0.02), controlled attenuation parameter (CAP) (B = 0.39, P = 0.049), and liver stiffness measurement (LSM) (B = 0.40, P = 0.03) in females. Higher waist to hip ratio was also significantly related to serum AST (B = 0.37, P = 0.04), ALT (B = 0.50, P = 0.02), CK18 (B = 0.41, P = 0.03), cCK18 (B = 0.37, P = 0.04), and CAP (B = 0.39,

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“…So, FAEEs are sufficient but not necessary for pancreatic injury. Given that free fatty acids are significantly increased in NAFPD/NASH, it is plausible that they may also mediate the pancreatotoxic effects of EE [13, [106][107][108][109].…”

Section: Discussionmentioning

confidence: 99%

“…Notwithstanding, it is known that healthy subjects not exposed to exogenous ethanol have endogenous trace of FAEEs in body fluids [103,104]. As the two substrates required for FAEEs biosynthesis, ethanol [68][77] [105] and free fatty acids [13, [106][107][108][109], are significantly elevated in NASH/NAFPD body fluids, it is quite possible they are formed in toxic amounts in the pancreas and oro-gastrointestinal tract.…”

Section: Endogenous Production Of Fatty Acid Ethyl Esters (Faee)mentioning

confidence: 99%

Nonalcoholic fatty pancreas disease as an endogenous alcoholic fatty pancreas disease

Medeiros¹,

Lima²

2016

Gastroenterol Hepatol Endosc

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Nonalcoholic fatty pancreas disease (NAFPD) is closely linked to nonalcoholic steatohepatitis (NASH), suggesting that the two conditions share a common etiopathogenetic background. In Addition, growing evidence indicates that endogenous ethanol (EE) plays a fundamental role in NASH pathogenesis. Accordingly, it is intuitively appealing to assume that EE plays also a causative role in NAFPD development. This connection is further supported by the finding that NAFPD shares with alcoholic fatty pancreas disease (AFPD) similar metabolic signaling pathways and histopathological features. However, low blood alcohol concentrations (BAC) along with the alleged inability of gut microbiota to produce toxic amounts of ethanol are the main obstacles to validate the idea of an endogenous alcoholic fatty pancreas disease (EAFPD). Here, we provide a mechanistic explanation reconciling the EAFPD hypothesis with these apparently conflicting observations. The key conclusions of our investigation are as follows. First, ethanol is a prodrug, implicating that under extensive presystemic metabolism BACs can be low and/ or absent. Second, oro-gastrointestinal microbiota may produce higher amounts of ethanol than those required to cause AFPD. Last, livers of NASH/NAFPD individuals overexpress all genes encoding alcohol-metabolizing enzymes identically to livers of patients with alcoholic hepatitis. Even more importantly, the upregulation of these genes is higher in the early steatotic stage of nonalcoholic fatty liver disease than in alcoholic hepatitis. This suggests a greater exposure of the liver, and by extension, of the pancreas, to ethanol in the former than in the latter condition. In summary, this paper provides a mechanistic framework for how NAFPD indeed may be an EAFPD.

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Palmitoleic acid is elevated in fatty liver disease and reflects hepatic lipogenesis

Abstract: The current data provide support for the use of the VLDL-triacylglycerol 16:1n-7 molar percentage as a biomarker for elevated liver fat when isotope use is not feasible; however, larger-scale confirmatory studies are needed.

Cited by 137 publications

References 62 publications

Is Palmitoleic Acid a Plausible Nonpharmacological Strategy to Prevent or Control Chronic Metabolic and Inflammatory Disorders?

Is Palmitoleic Acid a Plausible Nonpharmacological Strategy to Prevent or Control Chronic Metabolic and Inflammatory Disorders?

Interpretation of Serum Visfatin Level in Relation to Hepatic Injury is Probably Gender Dependent in Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty pancreas disease as an endogenous alcoholic fatty pancreas disease

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