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Chenxi Li,1,&ast; Xiaolei Chen,2,&ast; Xiaowen Zhu,1 Mengjiao Cao,3 Qunfeng Tang,3 Wenjun Wu1,4 1Department of Endocrinology, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, People’s Republic of China; 2Department of Neurology, Jiangnan University Medical Center, Wuxi No. 2 People’s Hospital, Wuxi, People’s Republic of China; 3Department of Radiology, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, People’s Republic of China; 4Jinshan Branch of Shanghai Sixth People’s Hospital, Shanghai, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Wenjun Wu, Department of Endocrinology, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, 214023, People’s Republic of China, Tel +86-15358008856, Fax +86-510-85737592, Email wuwenjung@163.comPurpose: Arterial stiffness is often increased in overweight or obese individuals before the development of hypertension (HT). This study aimed to determine the connection between pancreatic fat and atherosclerosis in overweight and obese people without HT.Patients and methods: We included 128 patients who were non-hypertensive and overweight or obese in a study between December 2019 and November 2022. Medical history was collected, and all participants underwent a physical examination and blood tests. Pancreatic fat content was measured by magnetic resonance imaging (MRI) and was grouped into quartiles based on pancreatic fat fraction (PFF). The upper three quartiles (PFF≥ 10.33%) were defined as non-alcoholic fatty pancreas disease (NAFPD) and the first quartile (PFF< 10.33%) as non-NAFPD. High baPWV (H-baPWV) and low baPWV (L-baPWV) were classified according to the median baPWV (1159 cm/s). The effect of NAFPD on baPWV was examined using binary logistic regression. The study population consisted of 96 NAFPD and 32 non-NAFPD cases.Results: Participants with NAFPD had significantly higher levels of baPWV than people without. The rates of NAFPD and the PFF values varied significantly in the L-baPWV and H-baPWV groups. Logistic regression analysis suggested that the presence of NAFPD was independently correlated with increased baPWV after adjusting for age, smoking, body mass index, blood pressure, lipid profiles, and glycemic index.Conclusion: NAFPD is an independent risk factor for increased baPWV in individuals with overweight and obesity but no HT, suggesting that the presence of NAFPD may be a warning signal of early atherosclerosis.Keywords: obesity, non-alcoholic fatty pancreas disease, overweight, arterial stiffness, brachial-ankle pulse wave velocity

ObjectiveThis retrospective observational study investigates the heterogeneity of hepatic and pancreatic fat deposition and its implications for metabolic health in individuals with obesity.MethodsA total of 706 patients with obesity underwent an MRI to quantify liver and pancreatic fat. Patients were classified into four groups based on fat deposition: no fat (None), fatty pancreas only (NAFPD), fatty liver only (NAFLD), and both conditions (NAFLD+NAFPD). Biochemical profiles, insulin resistance (Homeostatic Model Assessment for Insulin Resistance, HOMA-IR), and β-cell function were analyzed. A series of multiple linear regressions were used to investigate the independent effects of characteristics on glucose, insulin, and C-peptide at 0h. Another multiple linear regression was performed to evaluate the effects of basic characteristics on average liver fat, mean pancreatic fat, and visceral fat.ResultsThe majority (76.63%) exhibited both NAFLD and NAFPD, highlighting the heterogeneity of fat deposition among individuals with obesity. Groups with fatty liver displayed significantly higher fasting glucose, insulin, C-peptide, and HOMA-IR levels than those without fatty liver (P < 0.01). Fatty pancreas alone did not significantly influence these metabolic parameters (P > 0.05). This underscores the greater metabolic impact of hepatic fat compared to pancreatic fat.ConclusionsThe study confirms the complex heterogeneity of fat deposition in obesity, with the fatty liver being a more influential factor in metabolic disturbances than the fatty pancreas. The prevalent co-occurrence of NAFLD and NAFPD in this population underscores the need for targeted management strategies focusing on hepatic fat reduction to mitigate metabolic risk.

Antonia Pagkali,1 Anastasios Makris,1 Kalliopi Brofidi,2 Aris P Agouridis,3,4 Theodosios D Filippatos2 1School of Medicine, National and Kapodistrian University of Athens, Athens, Greece; 2Department of Internal Medicine, School of Medicine, University of Crete, Heraklion, Greece; 3School of Medicine, European University Cyprus, Nicosia, Cyprus; 4Department of Internal Medicine, German Oncology Center, Limassol, CyprusCorrespondence: Theodosios D Filippatos, Department of Internal Medicine, School of Medicine, University of Crete, Heraklion, Greece, Tel + (30)2810392960, Fax + (30)2810392359, Email filtheo@uoc.grAbstract: Non-Alcoholic Fatty Pancreas disease (NAFPD), characterized by fat accumulation in pancreatic tissue, is an emerging clinical entity. However, the clinical associations, the underlying molecular drivers, and the pathophysiological mechanisms of NAFPD have not yet been characterized in detail. The NAFPD spectrum not only includes infiltration and accumulation of fat within and between pancreatic cells but also involves several inflammatory processes, dysregulation of physiological metabolic pathways, and hormonal defects. A deeper understanding of the underlying molecular mechanisms is key to correlate NAFPD with clinical entities including non-alcoholic fatty liver disease, metabolic syndrome, diabetes mellitus, atherosclerosis, as well as pancreatic cancer and pancreatitis. The aim of this review is to examine the pathophysiological mechanisms of NAFPD and to assess the possible causative/predictive risk factors of NAFPD-related clinical syndromes.Keywords: non-alcoholic fatty pancreas disease, NAFPD, steatotic pancreatic disease, metabolic dysfunction-associated steatotic pancreatic disease, MASPD

The prevalence of non-alcoholic fatty pancreas disease (NAFPD) is estimated as 2–46% among patients without known pancreatic diseases. An association between NAFPD and non-alcoholic fatty liver disease (NAFLD) has been proposed, as well as an association between NAFPD and pancreatic exocrine insufficiency (PEI). Patients with histologically confirmed NAFLD were included in the study. The control group consisted of individuals included in a surveillance screening program. Magnetic resonance imaging (MRI) of the pancreas was performed in all patients and fat measurement was made using 2-point Dixon imaging. Fecal elastase-1 (FE-1) was performed to evaluate pancreatic exocrine function. Additionally, a 13C-mixed triglyceride breath test (13 C-MTG-BT) was performed in patients with FE-1 < 200 μg/g. Imaging signs of NAFPD were present in 17 (71%) patients; 11 (85%) from the NAFLD group and 6 (55%) from the control group. FE-1 < 200 μg/g was found in six (25%) patients (four in the NAFLD group and two in the control group); however, none of them had clinical symptoms of PEI. Therefore, in five out of six patients with low FE-1, a 13C-MTG-BT was performed, showing normal results (>20.9%) in all tested patients. Furthermore, the serum nutritional panel was normal in all patients with low FE-1. A systematic review identified five studies relevant to the topic. NAFPD was found in 85% of patients with NAFLD and in 55% of control patients. We did not diagnose PEI in either group. A literature review showed PEI in 9–56% of patients with NAFPD. [ABSTRACT FROM AUTHOR]

Purpose: To establish a simple and clinically useful method for the visual assessment of pancreatic fat deposition using computed tomography (CT) images, and to evaluate the relationship of the pancreatic fat deposition with body mass index (BMI) and type 2 diabetes mellitus (DM). Materials and methods: We used a four-scale grading system as the visual assessment criteria for pancreatic fat deposition using CT images. Pancreatic fat deposition was assessed for 200 patients and the results were compared with the CT attenuation-based assessment. In addition, the relationships of pancreatic fat deposition with BMI and type 2 DM were investigated. Results: The visual and CT attenuation-based assessments were considered consistent. The results of the visual assessment suggested that mild and moderate pancreatic fat deposition correlated with BMI and presence of type 2 DM while severe fat deposition did not correlate with them. No correlation between pancreatic fat deposition and HbA1c level was found. Conclusion: The visual assessment criteria we used were consistent with CT attenuation-based assessment and may be useful for clinical application of pancreatic fat deposition. According to the visually assessment, mild or moderate pancreatic fat deposition correlated with BMI and the presence of type 2 DM, but severe fat deposition did not correlate with them. [ABSTRACT FROM AUTHOR]

Objective: Fat accumulation in the liver and pancreas are clinical manifestations of metabolic syndrome associated with inflammation. It aimed to investigate the effects of the computed tomography (CT) estimated non-alcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreas disease (NAFPD) on the development of acute pancreatitis in this study. Patients and methods: This retrospective and cross-sectional study consisted of 194 participants admitted to the hospital with an abdominal pain complaint and underwent an abdominal CT scan during the investigation of the differential diagnosis. Medical database records of patients were investigated. Groups were consisted of according to the presence of acute pancreatitis as study and control. Attenuation measurements of the liver and pancreas were determined according to abdominal CT. Results: A statistical significance was observed for the development of acute pancreatitis when patients with normoglycemia were compared to patients with prediabetes and diabetes. Percentages of NAFLD and NAFPD according to the median of CT attenuation difference between pancreas and spleen values were elevated in the study group. A logistic regression model revealed that prediabetes, type 2 diabetes, NAFLD, and NAFPD, according to median value, were risk factors for acute pancreatitis (p<0.001, =0.001, =0.02, and =0.022). Discussion: NAFLD and NAFPD, according to the median value of patients without pancreatitis, were determined as independent risk factors for the development of acute pancreatitis. [ABSTRACT FROM AUTHOR]

Many breast cancer patients have both non-alcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreas disease (NAFPD). Consequently, we hypothesized that NAFPD and NAFLD were associated with breast cancer, and aimed to build a novel risk-stratification scoring system based on it. In this study, a total of 961 patients with breast cancer and 1,006 non-cancer patients were recruited. The clinical characteristics were collected and analyzed using logistic analysis. Risk factors were assessed by a risk rating system. Univariate analysis showed that body mass index, triglyceride, total cholesterol, NAFLD, NAFPD, low-density lipoprotein, and uric acid (UA) were significantly related to breast cancer. Among them, NAFLD, NAFPD, and UA were independent risk factors related to breast cancer identified by multivariate analysis. The risk assessment model was established based on these factors and demonstrated that the odds ratio sharply increased with the rising scores. Compared with the low-risk group, the odds ratio in the intermediate- and high-risk groups were 1.662 (1.380–2.001) and 3.185 (2.145–4.728), respectively. In conclusion, the risk-stratification scoring system combining NAFLD, NAFPD, and UA can accurately predict the occurrence of breast cancer.

Objective To investigate the correlation between pancreatic fat deposition and metabolic syndrome (MetS) parameters, focusing on the locations of fat deposition in the pancreas and sex differences. Methods Degrees of fat deposition in the head, body, and tail of the pancreas were evaluated using computed tomography (CT). We examined the relationships between pancreatic fat deposition and the age, body mass index (BMI), visceral and subcutaneous fat, serum lipid profiles, hepatic steatosis, diabetes mellitus (DM), and hypertension (HTN). Results In this retrospective study, greater fat deposition was associated with a higher BMI, visceral and subcutaneous fat accumulation, and hepatic steatosis, with the pancreatic head showing the strongest correlation. Correlations of pancreatic fat deposition with the BMI and visceral and subcutaneous fat accumulation were stronger in females than in males, while correlations with hepatic steatosis were stronger in males than in females. In addition, a multivariate analysis did not suggest a direct causal relationship between pancreatic fat deposition and DM and HTN, but there was a significant correlation between pancreatic fat deposition in the pancreatic head and visceral fat area. Conclusion Pancreatic fat deposition, as evaluated by CT, especially in the part of the pancreatic head adjacent to the ampulla of Vater, is a sensitive indicator of MetS. The correlations between pancreatic fat deposition and MetS parameters tended to be stronger in females than in males. These results may help further elucidate the pathophysiology of MetS and provide opportunities for its diagnosis.

Background and Aim: Obesity, insulin resistance, and metabolic alterations increase the risk of colorectal cancer and adenoma (CRA). Non‐alcoholic fatty liver disease (NAFLD) or pancreatic disease (NAFPD) shares many risk factors with CRA that may have significant roles in its development; however, the relationship between CRA and NAFLD/NAFPD remains unclear. Methods: This cross‐sectional study recruited 712 eligible participants without current drinking who had undergone total colonoscopy as part of a health checkup. These participants were classified into a CRA group (n = 236) and a control group (n = 439), which consisted of individuals without CRA and a history of polyp resection. NAFLD and NAFPD were diagnosed based on abdominal ultrasonography findings. Results: Non‐alcoholic fatty liver disease was observed more frequently in individuals with CRA than in the control group (55.9% vs 41.6%, P < 0.01). There was no significant association between NAFPD and CRA; however, serum pancreatic amylase (P‐amylase) levels were significantly lower in individuals with CRA. Although NAFLD was one of the factors increasing the presence of CRA (odds ratio [OR], 1.50; 95% confidence interval [CI], 1.07–2.10), low P‐amylase levels were significantly associated with the presence of CRA (OR, 1.73; 95% CI, 1.04–2.88) independent of age, sex, current smoking, obesity, metabolic alterations including insulin resistance, and NAFLD. Conclusions: Low serum P‐amylase levels were a possible independent risk factor for CRA in the present study. The latent pancreatic exocrine–endocrine–gut relationship was considered a novel pathway involved in obesity‐related CRA development, in non‐alcoholic individuals. [ABSTRACT FROM AUTHOR]

Many breast cancer patients have both nonalcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreas disease (NAFPD). Consequently, we hypothesized that NAFPD and NAFLD were associated with breast cancer, and aimed to build a novel risk-stratification scoring system based on it. In this study, a total of 961 patients with breast cancer and 1,006 non-cancer patients were recruited. The clinical characteristics were collected and analyzed using logistic analysis. Risk factors were assessed by a risk rating system. Univariate analysis showed that body mass index, triglyceride, total cholesterol, NAFLD, NAFPD, low-density lipoprotein, and uric acid (UA) were significantly related to breast cancer. Among them, NAFLD, NAFPD, and UA were independent risk factors related to breast cancer identified by multivariate analysis. The risk assessment model was established based on these factors and demonstrated that the odds ratio sharply increased with the rising scores. Compared with the low-risk group, the odds ratio in the intermediate- and high-risk groups were 1.662 (1.380–2.001) and 3.185 (2.145–4.728), respectively. In conclusion, the risk-stratification scoring system combining NAFLD, NAFPD, and UA can accurately predict the occurrence of breast cancer. [ABSTRACT FROM AUTHOR]

Fat accumulation in the pancreas associated with obesity and the metabolic syndrome (MetS) has been defined as "non-alcoholic fatty pancreas disease" (NAFPD). The aim of this review is to describe the association of NAFPD with obesity, MetS, type 2 diabetes mellitus (T2DM) and atherosclerosis and also increase awareness regarding NAFPD. Various methods are used for the detection and quantification of pancreatic fat accumulation that may play a significant role in the differences that have been observed in the prevalence of NAFPD. Endoscopic ultrasound provides detailed images of the pancreas and its use is expected to increase in the future. Obesity and MetS have been recognized as NAFPD risk factors. NAFPD is strongly associated with non-alcoholic fatty liver disease (NAFLD) and it seems that the presence of both may be related with aggravation of NAFLD. A role of NAFPD in the development of "prediabetes" and T2DM has also been suggested by most human studies. Accumulation of fat in pancreatic tissue possibly initiates a vicious cycle of beta-cell deterioration and further pancreatic fat accumulation. Additionally, some evidence indicates a correlation between NAFPD and atherosclerotic markers (e.g., carotid intima–media thickness). Weight loss and bariatric surgery decreases pancreatic triglyceride content but pharmacologic treatments for NAFPD have not been evaluated in specifically designed studies. Hence, NAFPD is a marker of local fat accumulation possibly associated with beta-cell function impairment, carbohydrate metabolism disorders and atherosclerosis. [ABSTRACT FROM AUTHOR]

Background Obesity is a major health problem worldwide, and non-alcoholic fatty pancreas disease (NAFPD) and non-alcoholic fatty liver disease (NAFLD) are obesity-associated complications. Liraglutide, a glucagon-like peptide-1 (GLP-1) agonist, has been approved for treatment of obesity. We aimed to evaluate the therapeutic effects of liraglutide on the complications through its regulation of endoplasmic reticulum (ER) stress. Methods A high-fat diet mouse model was established in C57BL/6J mice. Two groups of mice were fed a high-fat diet with 60% fat for 16 weeks and control mice were fed standard chow. A four-week 0.6 mg/kg/day liraglutide treatment was started in one high-fat diet group after 12 weeks of the high-fat diet. After sacrificing the mice, pancreatic and hepatic tissues were prepared for western blot and immunohistochemistry for ER stress proteins, including activating transcription factor 4 (ATF4), caspase 12, C/EBP homologous protein (CHOP) eukaryotic initiation factor 2 α (eIF2α), glucose regulated protein (GRP) 78 and protein kinase RNA-like endoplasmic reticulum kinase (PERK). Results Liraglutide significantly decreased body weight gained by mice consuming a high-fat diet (27.6 g vs. 34.5 g, P<0.001), and levels of all ER proteins increased significantly in both the pancreas and liver (all P<0.05). Expression of most ER stress proteins in pancreatic tissue correlated with disease scores of NAFLD (all P<0.05). However, no significant differences were found in pancreatic ATF 4 expression between mice without NAFLD, and those with early non-alcoholic steatohepatitis (NASH) and fibrotic NASH (P=0.122). Conclusion Liraglutide may reduce the severity of NAFPD and NAFLD through regulating the ER stress pathway and downstream apoptosis signaling. [ABSTRACT FROM AUTHOR]

Objective Pancreatic steatosis is associated with impaired beta cell function in patients with prediabetes. The pathomechanisms underlying this association still remain to be elucidated. Recent data show that adipocytes are situated within the pancreatic parenchyma and therefore give raise to hypothesize that pancreatic fat together with known and unknown metabolites such as hepatokines affect insulin secretion. Applying a targeted metabolomic approach we investigated possible circulating markers of pancreatic fat in order to better understand its role in the pathophysiology of impaired beta cell function. Methods We included 361 Caucasians, at increased risk of type 2 diabetes, from the Tübingen Family Study. All participants underwent a frequently sampled oral glucose tolerance test to assess insulin secretion and a magnetic resonance imaging to quantify pancreatic fat content, total body fat and visceral fat. Among the 152 subjects with prediabetes (IFG and/or IGT), two groups each with 20 individuals, having the lowest and highest pancreatic fat content were selected. The groups were matched for sex, age, BMI, total fat content, visceral fat content, liver fat content and insulin sensitivity. Metabolites were analyzed using the AbsoluteIDQ® p400 HR Kit by Biocrates. Results Pancreatic fat content of all 152 subjects with prediabetes was negatively associated with insulin secretion represented by AUCC-peptide 0–120 /AUCGlucose 0–120 (p=0.04; β=− 3.24). Furthermore, pancreatic fat content was positively associated with BMI, total body and visceral fat (all p<0.005). Levels of aminoacids, biogenic amines and monosaccharides were similar between the groups with high/low pancreatic fat content (p>0.90). Also, levels of polar lipids such as lysophosphatidylcholines, phosphatidylcholines, sphingomyelins and ceramides did not differ significantly between the groups (p>0.90). Investigating the levels of neutral lipids such as aclycarnitines, diglycerides, triglycerides and cholesteryl esters also revealed no differences between the groups (p>0.90). Conclusion The amount of pancreatic fat is not associated with the metabolomic pattern in individuals with prediabetes. This might be due to the relatively low pancreatic fat content compared to the total amount of fat stored in other depots. The impact of pancreatic steatosis on insulin secretion might be mediated by paracrine effects which cannot be detected in the circulation. [ABSTRACT FROM AUTHOR]

Context: Pancreatic steatosis leading to beta-cell failure might be involved in type 2 diabetes (T2D) pathogenesis.Objective: We hypothesized that the genetic background modulates the effect of pancreatic fat on beta-cell function and investigated genotype × pancreatic fat interactions on insulin secretion.Design: Two observational studies.Setting: University hospital.Patients or Participants: A total of 360 nondiabetic individuals with elevated risk for T2D (Tuebingen Family Study [TUEF]), and 64 patients undergoing pancreatectomy (Pancreas Biobank [PB], HbA1c <9%, no insulin therapy).Main Outcome Measures: Insulin secretion calculated from 5-point oral glucose tolerance test (TUEF) and fasting blood collection before surgery (PB). A genome-wide polygenic score for T2D was computed from 484,788 genotyped variants. The interaction of magnetic resonance imaging-measured and histologically quantified pancreatic fat with the polygenic score was investigated. Partitioned risk scores using genome-wide significant variants were also computed to gain insight into potential mechanisms.Results: Pancreatic steatosis interacted with genome-wide polygenic score on insulin secretion (P = 0.003), which was similar in the replication cohort with histological measurements (P = 0.03). There was a negative association between pancreatic fat and insulin secretion in participants with high genetic risk, whereas individuals with low genetic risk showed a positive correlation between pancreatic fat and insulin secretion. Consistent interactions were found with insulin resistance-specific and a liver/lipid-specific polygenic scores.Conclusions: The associations suggest that pancreatic steatosis only impairs beta-cell function in subjects at high genetic risk for diabetes. Genetically determined insulin resistance specifically renders pancreatic fat deleterious for insulin secretion. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a common disorder with an increasing prevalence, characterised by persistent respiratory symptoms and airflow limitation. Systemic inflammation is involved in the pathogenesis of COPD and can also predispose to metabolic disorders (e.g., metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD)). Such comorbidities can negatively affect COPD outcomes, cardiovascular risk, and quality of life. Apart from NAFLD, abnormal peri-organ or intra-organ fat (APIFat) could be considered as markers for cardiometabolic diseases and even for COPD. The present narrative review considers the associations of COPD with MetS, NAFLD, and other APIFat, including epicardial, perirenal, peripancreatic, and intramuscular adipose tissue. Further research is needed to define these relationships and identify any potential clinical implications.

With the increasing global epidemic of obesity, the clinical importance of non-alcoholic fatty pancreas disease ( NAFPD) has grown. Even though the pancreas might be more susceptible to ectopic fat deposition compared with the liver, NAFPD is rarely discussed because of the limitation of detection techniques. In the past, NAFPD was considered as an innocent condition or just part of clinical manifestations during the course of obesity. Recently, a growing body of research suggests that NAFPD might be associated with β-cell dysfunction, insulin resistance and inflammation, which possibly lead to the development of diabetes and metabolic syndrome. The present review summarized the current literature on the epidemiology, potential pathophysiology, diagnostic techniques, impact of NAFPD on β-cell function and insulin resistance, and the clinical relevance of the interplay between NAFPD and glucometabolic disorders. [ABSTRACT FROM AUTHOR]

The author reflects on non-alcoholic fatty pancreas disease (NAFD) by citing a study on patients with both hepatic steatosis (HS) and NAFD. Based on the results, the patients showed greater carotid intima media thickness (cIMT) compared to patients with HS only. Other topics include non-alcoholic fatty liver disease (NAFLD) and the abnormal peri-organ or intra-organ fat (APIFat) deposition as risk factor for metabolic and vascular diseases.

Characterising the molecular networks that negatively regulate pancreatic β-cell function is essential for understanding the underlying pathogenesis and developing new treatment strategies for type 2 diabetes. We recently identified serine/threonine protein kinase 25 (STK25) as a critical regulator of ectopic fat storage, meta-inflammation, and fibrosis in liver and skeletal muscle. Here, we assessed the role of STK25 in control of progression of non-alcoholic fatty pancreas disease in the context of chronic exposure to dietary lipids in mice. We found that overexpression of STK25 in high-fat-fed transgenic mice aggravated diet-induced lipid storage in the pancreas compared with that of wild-type controls, which was accompanied by exacerbated pancreatic inflammatory cell infiltration, stellate cell activation, fibrosis and apoptosis. Pancreas of Stk25 transgenic mice also displayed a marked decrease in islet β/α-cell ratio and alteration in the islet architecture with an increased presence of α-cells within the islet core, whereas islet size remained similar between genotypes. After a continued challenge with a high-fat diet, lower levels of fasting plasma insulin and C-peptide, and higher levels of plasma leptin, were detected in Stk25 transgenic vs wild-type mice. Furthermore, the glucosestimulated insulin secretion was impaired in high-fat-fed Stk25 transgenic mice during glucose tolerance test, in spite of higher net change in blood glucose concentrations compared with wild-type controls, suggesting islet β-cell dysfunction. In summary, this study unravels a role for STK25 in determining the susceptibility to diet-induced nonalcoholic fatty pancreas disease in mice in connection to obesity. Our findings highlight STK25 as a potential drug target for metabolic disease. [ABSTRACT FROM AUTHOR]

Objective Growing evidence suggests that individuals with excessive fat in the pancreas are at an increased risk of chronic metabolic disorders. The aim was to systematically review studies on non-alcoholic fatty pancreas disease (NAFPD) with a view to determine its prevalence, associations with metabolic co-morbidities, and to suggest normal pancreatic fat percentage threshold. Methods Three electronic databases (MEDLINE, Scopus, and Embase) were queried. Studies in humans were eligible for inclusion if they provided data on NAFPD and/or pancreatic fat percentage. Where possible, data were pooled using random-effects meta-analysis and the effect of covariates analysed using meta-regression. Results Pooling data on pancreatic fat percentage from nine studies (1209 healthy individuals who underwent magnetic resonance imaging), yielded the weighted mean and weighted standard deviation of 4.48% and 0.87%, respectively. Pooling data on NAFPD from eleven studies (12,675 individuals), yielded the pooled prevalence of 33% (95% confidence interval, 24% - 41%). Meta-regression analysis showed that the prevalence of NAFPD was independent of age and sex. The presence of NAFPD was associated with a significantly increased risk of arterial hypertension (risk ratio 1.67; 95% confidence interval, 1.32–2.10; p < 0.0001), diabetes mellitus (risk ratio 2.08; 95% confidence interval, 1.44–3.00; p = 0.0001), and metabolic syndrome (risk ratio 2.37; 95% confidence interval, 2.07–2.71; p < 0.0001). Conclusion The findings indicate that NAFPD is a frequent clinical entity, associated with significantly increased risk of metabolic syndrome and its components. The normal pancreatic fat cut-off point of 6.2% may be recommended for use in future prospective studies. [ABSTRACT FROM AUTHOR]

Background: The clinical significance of non-alcoholic fatty pancreatic disease (NAFPD) or fatty pancreas is largely unknown. It is often an incidental finding on abdominal ultrasound, which is not explored further, especially its association with metabolic condition and the risk of pancreatic malignancy. The aim of this study is to evaluate the presence of NAFPD and its associated risk factors among adult medical check-up patients.Method: A large cross-sectional study was done among adult medical check-up patients underwent abdominal ultrasound between January and December 2013 in Medistra Hospital, Jakarta. Data was obtained from the patients' medical record and include demographic data, blood pressures, fasting blood glucose level, and lipid profile. The presence of fatty pancreas was diagnosed by ultrasound. Bivariate and multivariate analyses were done to find associated risk factors for NAFPD. Statistical analysis was done using SPSS version 17.Results: A total of 1054 cases were included in this study; pancreas cannot be visualized in 153 cases and were excluded from the analysis. Fatty pancreas was present in 315 (35.0%) patients. Bivariate analyses found associations among fatty pancreas and several risk factors such as gender, age, systolic and diastolic blood pressures, body mass index (BMI), fasting plasma glucose (FPG), triglycerides (TG) and cholesterol levels.Conclusion: Fatty pancreas is a common finding during medical check-up with a prevalence of 35%. Fatty pancreas has significant association with metabolic factors and it might have an important role in risk of malignancy. [ABSTRACT FROM AUTHOR]

Background: Evidence that individuals with excess fat in the pancreas have an increased risk of cardiovascular disease has been growing recently. Risk evaluation in acute coronary syndrome (ACS) patients plays a crucial role for both prognosis prediction and decision-making., Aim: The main aim of this study was to investigate the relationship between non-alcoholic fatty pancreas disease (NAFPD) and the complexity and severity of coronary artery disease as assessed using the SYNTAX score (SXscore) in ACS patients., Methods: A total of 99 consecutive patients with a first-time diagnosis of ACS were recruited. NAFPD was evaluated using transabdominal ultrasonography (TUS). SXscore was calculated using the SXscore algorithm., Results: The patients with NAFPD had a significantly higher SXscore than those without NAFPD (12.3 ± 6.4 and 8.2 ± 4.3, p < 0.001). Univariable analysis showed that hypertension (p = 0.033) and presence of NAFPD (p = 0.001) were associated with increased SXscore. Moreover, multivariable analysis showed that the presence of NAFPD (p = 0.002) was associated with increased SXscore., Conclusions: NAFPD is easily detected by TUS. The presence of NAFPD in ACS patients may be a warning signal of complexity and severity of coronary artery disease.

Chronic obstructive pulmonary disease (COPD) is a common disorder with an increasing prevalence, characterised by persistent respiratory symptoms and airflow limitation. Systemic inflammation is involved in the pathogenesis of COPD and can also predispose to metabolic disorders (e.g., metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD)). Such comorbidities can negatively affect COPD outcomes, cardiovascular risk, and quality of life. Apart from NAFLD, abnormal peri-organ or intra-organ fat (APIFat) could be considered as markers for cardiometabolic diseases and even for COPD. The present narrative review considers the associations of COPD with MetS, NAFLD, and other APIFat, including epicardial, perirenal, peripancreatic, and intramuscular adipose tissue. Further research is needed to define these relationships and identify any potential clinical implications. [ABSTRACT FROM AUTHOR]

Objectives: Pancreas steatosis is the description of fat accumulation in the pancreatic gland. The prevalence and development mechanisms of pancreatic steatosis in patients with metabolic disorders still remain unclear. The aim of this study is to systematically review the association between pancreatic steatosis and metabolic co-morbidities.Methods: We performed a systematic search strategy using three electronic databases (MEDLINE, Scopus, and Embase) for relevant studies concerning the associations of pancreatic steatosis with metabolic syndrome (MetS) and its clinical relevance from inception until 30 September 2018.Results: One thousand three hundred fifty one references were identified in the initial search, and a total of 13 studies involving 49 329 subjects were included. This analyses elucidated the presence of non-alcoholic fatty pancreas disease (NAFPD) and was associated with a significant increased risk of metabolic syndrome (RR = 2.25; 95% CI, 2.00-2.53; P < 0.0001; I2  = 42.8%; eight studies included), hypertension (RR = 1.43; 95% CI, 1.08-1.90; P = 0.013; I2  = 94.7%; nine studies included), non-alcoholic fatty liver disease (NAFLD) (RR = 2.49; 95% CI, 2.06-3.02; P < 0.0001; I2  = 96.9%; nine studies included), diabetes mellitus (RR = 1.99; 95% CI, 1.18-3.35; P = 0.01; I2  = 97.6%; 10 studies included), and central obesity (RR = 1.91; 95% CI, 1.67-2.19; P < 0.0001; I2  = 95.9%; six studies included). The association between NAFPD and hyperlipidaemia was not statistically significant (RR = 1.33; 95% CI, 0.82-2.17; P = 0.249; I2  = 97%; five studies included).Conclusions: The existing evidence indicates that NAFPD is significantly associated with an increased risk of metabolic syndrome and its components. Well-designed prospective cohort studies between pancreatic steatosis and MetS are needed to elaborate the causality in the future. [ABSTRACT FROM AUTHOR]