Implications of Tobacco Smoking and Alcohol Consumption on Ectopic Fat Deposition in Individuals After Pancreatitis.

OBJECTIVES: Tobacco smoking and alcohol consumption are established risk factors for pancreatitis. This study investigated the associations between tobacco smoking/alcohol consumption in people after an attack of pancreatitis and intrapancreatic fat deposition (IPFD), intrahepatic fat deposition (IHFD), and skeletal muscle (SMFD) fat deposition. METHODS: In this cross-sectional study, magnetic resonance imaging was used to quantify IPFD, IHFD, and SMFD by 2 independent raters. A validated questionnaire was used to determine tobacco smoking and alcohol consumption. RESULTS: A total of 119 individuals after an attack of pancreatitis were included. Average tobacco smoking contributed most to variance in IPFD (R = 6.5%) and least to variance in SMFD (R = 0.4%). Average alcohol consumption contributed most to variance in variance in IPFD (R = 2.8%) and least to IHFD (R = 1.1%). Packs/day contributed more than years of smoking to variance in IPFD (R = 4.9 and 0.2%, correspondingly), whereas years of drinking contributed more than average daily alcohol consumption (R = 3.9 and 3.2%, correspondingly). CONCLUSIONS: Tobacco smoking and alcohol consumption contributed more to variance in IPFD than IHFD and SMFD. Smoking contributed more than drinking to variance in IPFD. The daily amount of tobacco smoked appeared to be more important than years of smoking for IPFD.

Associations Between Cannabis Use, Abdominal Fat Phenotypes and Insulin Traits.

BACKGROUND: General obesity has been linked to dysregulation of the endocannabinoid system in humans. However, there is a lack of studies on the relationship between cannabis use and specific abdominal fat phenotypes. The aim was to investigate the associations between cannabis use and magnetic resonance imaging-derived fat phenotypes, as well as indices of insulin sensitivity and insulin secretion. METHODS: In this cross-sectional study, magnetic resonance imaging was used to quantify subcutaneous fat volume (SFV), visceral fat volume (VFV), intra-hepatic fat deposition (IHFD), intra-pancreatic fat deposition (IPFD) and skeletal muscle fat deposition (SMFD) by two independent observers. Insulin sensitivity was determined based on HOMA-IS, Raynaud index and Matsuda index, whereas insulin secretion was determined based on HOMA-ß, insulinogenic index 30' and insulinogenic index 60'. A validated questionnaire was used to ascertain participants' cannabis use. Linear regression models were constructed, adjusting for demographics, glycated hemoglobin, physical activity, tobacco smoking and alcohol consumption. RESULTS: A total of 120 individuals were included. Cannabis use explained 9.2% of variance in IHFD, 4.4% in SMFD, 3.4% in VFV, 0.4% in SFV and 0.2% in IPFD. Regular cannabis users had significantly greater IHFD compared with never users, in both the unadjusted (P = 0.002) and all adjusted (P = 0.002; P = 0.008) analyses. The other fat phenotypes did not differ significantly between either regular or non-regular users compared with never users. Regular cannabis users had significantly greater insulin secretion (as defined by the insulinogenic index 60') compared with never users, in both the unadjusted (P = 0.049) and all adjusted (P = 0.003; P = 0.004) analyses. Cannabis use explained 20.3% of variance in the insulinogenic index 60', but was not significantly associated with the other indices of insulin secretion. There were no significant differences in indices of insulin sensitivity in either regular or non-regular cannabis users compared with never users. CONCLUSION: Regular cannabis use may be a risk factor for non-alcoholic fatty liver disease (but not IPFD) and may alter the neuromodulation of insulin secretion. Further investigations are now warranted to elucidate the mechanisms underlying these associations.

Psoas muscle size as a magnetic resonance imaging biomarker of progression of pancreatitis.

OBJECTIVE: Pancreatitis often represents a continuous inflammatory process, from the first episode of acute pancreatitis (FAP) to recurrent acute pancreatitis (RAP) to chronic pancreatitis (CP). Psoas muscle size is a validated surrogate for global skeletal mass, changes in which are associated with inflammation. The objective was to investigate psoas muscle size in individuals following FAP, RAP, and CP, as well as its associations with pro-inflammatory cytokines. METHODS: Individuals following pancreatitis and healthy individuals were recruited. All participants underwent magnetic resonance imaging, from which psoas muscle volume was derived independently by two raters in a blinded fashion. Circulating levels of four major cytokines (interleukin-6, tumour necrosis factor-α, C-C motif chemokine ligand 2, and leptin) were measured. Five linear regression additive models were built to adjust for possible confounders (age, sex, body composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and endocrine and exocrine pancreatic functions). RESULTS: A total of 145 participants were enrolled. A significant downward trend in psoas muscle volume was observed between healthy controls and individuals following FAP, RAP, and CP in all adjusted models (p = 0.047, 0.005, 0.004, and < 0.001). Leptin was significantly associated with psoas muscle volume in all models (ß = - 0.16, p = 0.030 in the most adjusted model). The other studied cytokines were not significantly associated with psoas muscle volume. CONCLUSIONS: Psoas muscle size is significantly reduced along the continuum from FAP to RAP to CP. Leptin appears to be one of the factors implicated in this. Further studies are warranted to investigate the relationship between skeletal muscle and inflammation of the pancreas. KEY POINTS: • First acute pancreatitis, recurrent acute pancreatitis, and chronic pancreatitis were associated with progressively reduced psoas muscle size. • The findings were independent of age, sex, body fat composition, physical activity, tobacco smoking, alcohol consumption, comorbidities, and exocrine and endocrine functions of the pancreas. • The mechanism underlying the observed findings may involve hyperleptinaemia.

Relationship of pancreas volume to tobacco smoking and alcohol consumption following pancreatitis.

BACKGROUND: Tobacco smoking and alcohol consumption are established risk factors for diseases of the pancreas. With the recent advances in imaging modalities (such as magnetic resonance (MR) imaging), opportunities have arisen to study pancreas size, in both health and disease. Studies investigating the relationship between tobacco smoking, alcohol consumption, and total pancreas volume (TPV) - a holistic measure of pancreatic exocrine reserve - are lacking. The aim of the present study was to investigate the associations between MR-derived TPV and tobacco smoking/alcohol consumption. METHODS: This cross-sectional study recruited individuals with a history of pancreatitis and healthy controls. A validated questionnaire was used to ascertain current and lifetime tobacco smoking and alcohol consumption. TPV was quantified using MR images by two independent raters. Generalized additive models and linear regression analyses were conducted and adjusted for demographic, metabolic, and pancreatitis-related factors. RESULTS: A total of 107 individuals following pancreatitis and 38 healthy controls were included. There was no statistically significant difference in TPV between any of the tobacco smoking/alcohol consumption categories of individuals following pancreatitis and healthy controls, in both unadjusted and adjusted analyses. In individuals following pancreatitis, multivariate linear regression found no association between TPV and 7 smoking- and alcohol-related variables. Sensitivity analyses constrained to individuals who did not abstain from either smoking or drinking following their first attack of pancreatitis did not yield statistical significance with TPV. In post-hoc analysis, age was significantly inversely associated with TPV in the most adjusted model (p = 0.016). CONCLUSIONS: This is the first study to investigate the association between tobacco smoking, alcohol consumption, and MR-derived TPV following pancreatitis. It appears that age, but not tobacco smoking or alcohol consumption, is associated with a significantly reduced TPV.

Circulating levels of lipocalin-2 are associated with fatty pancreas but not fatty liver.

Lipocalin-2 (LCN-2), a peptide with diverse expression pattern, has been identified as a biomarker of various diseases as well as a factor contributing to inflammatory responses associated with excess adiposity and ensuing metabolic disorders. Although the inter-relationship between LCN-2 and excess adiposity is increasingly recognized, little is known about the inter-relationship between LCN-2 and ectopic fat deposition. The present study aimed to investigate the associations between LCN-2 and fatty pancreas as well as fatty liver. In addition, the associations between LCN-2 and pro-inflammatory cytokines were studied. Magnetic resonance imaging was used to quantify intra-pancreatic fat deposition and visceral-to-subcutaneous fat volume ratio whereas magnetic resonance spectroscopy was used to quantify liver fat deposition. Fasting venous blood was analyzed for LCN-2, C-C motif chemokine ligand 2, interleukin-6, leptin, tumor necrosis factor-α, glycated hemoglobin, glucose, and insulin. Binary logistic regression and linear regression analyses were conducted. Three statistical models were built to adjust for demographics, comorbidities, levels of glycated hemoglobin, insulin resistance, and abdominal fat distribution. A total of 79 individuals were studied, of whom 20 had fatty pancreas, 14 had fatty liver, and 4 had both. Lipocalin-2 was significantly associated with fatty pancreas in all the adjusted models (p = 0.014 in the most adjusted model) but was not significantly associated with fatty liver in any of the studied models. Lipocalin-2 was significantly associated with interleukin-6 and tumor necrosis factor-α, in both the unadjusted and adjusted models. Leptin and C-C motif chemokine ligand 2 were not significantly associated with LCN-2 in any of the studied models. These findings suggest that LCN-2 is a potential biomarker of fatty pancreas, independent of abdominal fat distribution, insulin resistance, and other covariates. The role of LCN-2 in intra-pancreatic fat deposition and related low-grade inflammation warrants further investigations.