Metabolic syndrome and its components such as obesity, hypertriglyceridemia, type-2 diabetes mellitus (DM-T2), and arterial hypertension are unequivocally serious problems for every society. This is especially true in economically developed countries where the imbalance in lifestyle between caloric intake and caloric output still gets greater and greater. This fact is not only a concern for the adult population but for children as well. However, metabolic syndrome does not only affect society and health in regards to cardiovascular diseases, it significantly concerns gastroenterology where it is classified as nonalcoholic fatty pancreas disease (NAFPD). The data gained from several trials show that the prevalence of NAFDP is 33% (95% CI 24–41%). When it comes to the diagnostic procedures concerning the presence of pancreatic fat, a whole spectrum of suitable methods are recommended. Probably, the most exact method is the use of magnetic resonance imaging. However, for common clinical practice, the abdominal sonographic examination based on the comparison of the pancreatic parenchymatous echogenity versus renal or hepatic echogenity is used. The clinical consequences of pancreatic steatosis and steatopancreatitis are significant. These diseases are connected with DM-T2 and insulin resistance. In recent years, changes of exocrine pancreatic function, particularly its decrease, have also been described. It is known that there is a close correlation between NAFPD and nonalcoholic hepatic steatosis and also with the increased thickness of aortic intima-media. There is also an important relationship between NAFPD and pancreatic carcinoma. Pancreatic steatosis, and especially its NAFPD form, is a serious state which can be treatable by the possible effective management of metabolic syndrome parameters, including obesity.

Fatty storage in the pancreas is mentioned under various names. Similarly, the etiology of the state is various. Pancreatic steatosis was first described by Ogilvie [1]. In their set of observed obese patients, he described the presence of pancreatic fat in 17% of the obese patients, while in the slim patients, it was present only in 7%. In 1978, Olsen [2] examined a group of 394 autopsied patients and found an increased amount of pancreatic fat in a direct relationship to age. Similarly, Stamm [3] proved an increase of pancreatic fat associated with higher age. They also found a significant relationship between pancreatic steatosis when fatty content in the pancreas is at 25% or more, and the risk of development of type-2 diabetes mellitus (DM-T2) and atherosclerosis. In 2010, van Geenen et al. [4] expressed the hypothesis that obesity and its association with insulin resistance play an important role in pancreatic infiltration with adipocytes, leading to steatosis of the gland. Insulin resistance also leads to peripheral lipolysis, and subsequently to a flux of fatty acids into the hepatic parenchyma and the onset of nonalcoholic fatty liver disease (NAFLD).

Pezzilli and Calculli [5] assumed that the most suitable name for fatty accumulation in the pancreas is the term pancreatic steatosis. This term also characterizes the fatty accumulation in the pancreas as a reversible process. The terminology dealing with fatty accumulation in pancreatic tissue is clearly summarized in Table 1 (adjusted according to Smits and van Geenen [6, 7]). The epidemiological data are not numerous. Epidemiological trials performed between 2014 and 2016 state the prevalence of nonalcoholic fatty pancreas disease (NAFPD) as being between 16 and 35%. This is mostly based on the results gained in the Asian population [8-10]. Only one epidemiological trial which was published in 2016 [11] dealt with pediatric population and puts the prevalence of pancreatic steatosis at 10%. The limiting factor of this work is the fact that it was performed entirely on hospitalized children, not on the general pediatric population.

Table 1.

Nomenclature of the fat in the pancreas

Nomenclature of the fat in the pancreas
Nomenclature of the fat in the pancreas

There are basically 2 mechanisms leading to fatty accumulation in the pancreas [6].

The first is the death of acinar cells and their substitution by adipocytes. In this case, the state is called “fatty replacement”. The second is fatty accumulation called “fatty infiltration”. Both of these states are succeeded by the presence of DM-T2, metabolic syndrome, and/or obesity.

The risk induction factors of steatopancreatitis include:

(a) Congenital diseases (Shwachman-Diamond syndrome, Johanson-Blizzard syndrome, cystic fibrosis, heterozygous carboxyl-ester lipase mutation)

(b) Alcohol abuse

(c) Infections (viral infection with Reovirus)

(d) Hemochromatosis

(e) Medicines (rosiglitazone, corticosteroids, octreotide, gemcitabine)

(f) Malnutrition

(g) NAFLD, chronic hepatitis B?

(h) Necrotizing pancreatitis?, recurrent acute pancreatitis?, hereditary chronic pancreatitis?

One of the signs of the presence of risk factors is the manifestation of steatopancreatitis, which is evidently caused by different mechanisms. The trials performed on patients and animal trials show the coexistence of -NAFPD with NAFLD [4, 12]. Both NAFPD and NAFLD are closely connected with obesity and the increased presence of visceral adipose tissue [13, 14].

NAFPD is a disease where obesity or obesity as a part of metabolic syndrome is the essential risk factor. The experimental trials show that maternal obesity and postnatal obesogenic diet lead to the onset of NAFPD. The inductors are endoplasmic reticulum, disbalance, and the alteration of circadian metabolic processes [15]. In our clinical trial, we proved that metabolic syndrome and its components (obesity, arterial hypertension, hypertriglyceridemia, the changes of HDL cholesterol, and -DM-T2) are all significant factors of NAFPD development [16].

The generally true correlation between the finding of NAFPD and NAFLD is not however absolutely valid [13]. Although hepatic fat is localized mainly intracellularly, pancreatic fat is connected to the presence of adipocytes which infiltrate its parenchyma. Therefore, for example, during a bariatric surgical intervention, the mentioned hepatic fat and pancreatic fat change and disappear quite independently of each other [17]. Despite this, it cannot be ruled out that NAFPD and NAFLD influence each other regarding disease onset and progression.

There is not a clear consensus as to the diagnostic methods concerning the presence of pancreatic fat. The optimum method should be able to simultaneously determine the presence of fat in the gland and its quantity in a noninvasive way. The imaging methods play the most important role in diagnostics.

Transabdominal ultrasonographic examination is a noninvasive and widely available method. Pancreatic steatosis is defined as an image of increased echogenity in the pancreatic parenchyma, when compared with the renal echogenity or liver echogenity, where the possible presence of hepatic steatosis is the limitation of evaluation. Therefore, it is first recommended to compare the hepatic and renal echogenity and then, using the same acoustic window, compare the pancreatic echogenity with the renal or hepatic echogenity. With respect to the possible presence of hepatic steatosis, it seems to us that for this purpose comparison only with renal echogenity is better. One limitation of this type of examination can be excessive obesity, and it can be emphasized that the examination is operator dependent. The method for quantitative evaluation of pancreatic echogenity was not generally accepted [18].

Endoscopic ultrasound is an endoscopic invasive method, which enables a very good visualization and evaluation of the examined gland. The evaluation of texture in the pancreatic parenchyma is quite exceptional. Various trials have shown the relationship between increased pancreatic echogenity and the presence of fatty liver, obesity with BMI >30.0, and usually also with arterial hypertension and even age higher than >60 years [19, 20]. This method is also operator dependent. The increased echogenity of pancreatic parenchyma is not always the image of an increased fatty presence in the pancreas, but it can be caused by the presence of pancreatic fibrosis, which is considered as a method limitation [21].

Computed tomography. A typical fatty pancreas is hypodense in Hounsfield units compared to the spleen [22]. The method is operator dependent, and the evaluation of its diagnostic profit is not uniform [23, 24]. Saisho et al. [25], for example, found computed tomography examination using the evaluation of fat/parenchyma ratio to be a reliable method when compared with the histological diagnosis.

Magnetic resonance imaging (MRI) is the most preferred method at present. The advantage of MRI is its noninvasivity, safety, and high sensitivity. The various trials showed that its accuracy in the identification of fat presence is comparable with histological examination, and in this way, it is the preferred method in the diagnostics of pancreatic lipomatosis [17, 26].

MRI proton density fat fraction. This method enables a highly accurate quantification of the amount of fat present in the pancreatic parenchyma [27]. At present, this method is also indicated for the quantitative determination of fat in the adjacent parenchymatous organs, not only in a pancreas [28].

Ultrasound elastography can evaluate organ’s -stiffness. In pancreatology, it has been useful in diagnostics of pancreatic diseases, that is, elastography via endoscopic ultrasound predicts exocrine pancreatic insufficiency in chronic pancreatitis [29]. There are some limitations in diagnosing steatopancreatitis, especially the retroperitoneal location of the pancreas and its small size, which can decrease the diagnostic accuracy.

Metabolic Syndrome and Cardiovascular Diseases

Metabolic syndrome belongs to the serious civilizational diseases befalling around 30% of the population. After previous discussions concerning its definition, the so called harmonized definition of metabolic syndrome was accepted in 2009 which is characterized by the total of 5 components, the presence of 3 of which is necessary to make the diagnosis of metabolic syndrome [30]. The components of metabolic syndrome include DM with insulin resistance, arterial hypertension, obesity, and dyslipidemia (hypertriglycidemia, decrease of HDL cholesterol). Obesity is the main important factor which can be considered a pandemic across societies. Abdominal obesity is characterized by dysfunction of adipose tissue, when the metabolism of esterified fatty acids is altered and this, together with DM, is a risk factor for the development of cardiovascular diseases [31]. Adipose tissue is an important endocrine organ producing adipocytokines and inflammatory mediators, for example, TNF-alfa [32]. Because of that obesity is an important risk factor not only for cardiovascular diseases but also for gastrointestinal diseases, including afflictions of liver and pancreas.

Ectopic fat deposits are in close correlation with cardiovascular diseases, NAFLD and epicardial adipose tissue [33]. Kul et al. [34] published a trial where they observed the role of NAFPD, the presence of epicardial adipose tissue, and changes in the thickness of the aortic intima-media. They proved that the presence of NAFPD is connected with an increased occurrence of increased aortic intima-media thickness and epicardial adipose -tissue.

There is no doubt that metabolic syndrome and its components are in close correlation with NAFPD, as was confirmed in a trial evaluating 13 publications with a total of 49,329 subjects [35].

Insulin Resistance

The results of the trials performed evaluating the association between NAFPD and insulin resistance are still controversial. Della Corte et al. [36] found a higher level of insulin resistance, circulating tumor necrosis factor alpha, and interleukin 1beta only in obese children with NAFLD, but not in the children with NAFPD. Moreover, HOMA-insulin resistance was found in those patients with NAFPD namely in connection with a higher BMI [37]. However, these results are challenged by the scientific works published by Le et al. [38] and Rossi et al. [14], which show them to be controversial. The authors found a relationship between the content of pancreatic fat and markers of insulin resistance. The question is if pancreatic steatosis really is the cause of insulin resistance, or if it is only a part of the other possible etiological factors.

Type-2 Diabetes Mellitus

DM-T2, formerly known as noninsulin dependent or adult onset diabetes, belongs to the components of metabolic syndrome and its relationship to obesity and insufficient physical activity has been clearly described [39]. Some investigations have shown that fatty infiltration of the pancreas leads to the loss of beta cells and their function, which was designated as the driving force in the development of DM [40]. The most frequent explanation concerning the relationship between NAFPD and the dysfunction of pancreatic beta-cells is based on the glycolipotoxic phenomenon. Hyperglycemia in the beta cells inhibits the beta-oxidative mitochondrial process through a cascade of enzymatic processes, which ultimately leads to the intracellular accumulation of triglycerides as its final consequence. Insulin resistance simultaneously reduces the inhibitory insulin activity in lipolytic processes and leads to the increase of circulating free fatty acids [41]. Tushuizen et al. [42] evaluated the pancreatic fat content and beta cell function in men with and without DM-T2. The pancreatic fat content was compared between the diabetic patients and the controls. The fat content was significantly higher in the set of patients with DM [42]. Ou et al. [40] found an important relationship between -NAFPD and the development of prediabetes in men [39]. The negative association between the quantity of pancreatic fat and insulin secretion in patients with prediabetes was described by Heni et al. [13]. van der Zilj et al. [43] proved that those patients with prediabetes have a higher content of pancreatic fat; however, they did not find a relationship between fatty pancreas and insulin secretion.

Pancreatic Cancer

Publications documenting the influence of obesity and insufficient physical activity on the development of various tumorous diseases including those of the pancreas began to appear as early as in the first decade of this century [44, 45]. The presence of the pancreatic inflammatory process in the terrain of pancreatic steatosis is the most important predisposing factor for the development of pancreatic adenocarcinoma [46]. The carcinogenetic mechanism in fatty pancreas has still not been fully -elucidated.

In 2017, Lesmana et al. [47] showed an increased prevalence of NAFPD in his set of patients suffering from pancreatic carcinoma. He evaluated NAFPD as one of the significantly important risk factors for the development of pancreatic carcinoma.

Various authors focusing on patients who were operated on for ductal pancreatic adenocarcinoma reported significantly higher risk of postoperative complications, mainly the development of pancreatic fistulas, in association with increased presence of fat in the pancreatic tissue [48-50].

Exocrine and Endocrine Pancreatic Functions

The relationship between pancreatic steatosis, steatopancreatitis, and pancreatic functional disorder is attributed to beta-cell lipotoxicity [22]. Furthermore, as proven by Pezzilli and Calculli [5], a close relationship also exists between obesity and steatopancreatitis, and obesity and DM-T2. In the trial of Miyake et al. [51], the authors confirmed that the presence of a fatty pancreas is an independent risk factor, extremely important for the relationship with endocrine pancreatic function. Therefore, it is necessary to further study the clinical course of patients with endocrine pancreatic impairment due to a fatty pancreas.

Exocrine pancreatic insufficiency can be defined as insufficient activity of pancreatic enzymes in the duodenum as a result of insufficient pancreatic secretion or premature enzyme destruction. The other conditions associated with exocrine pancreatic insufficiency include chronic pancreatitis, pancreatic carcinoma, coeliac disease, DM, or pancreatic resection. Pancreatic steatosis can also be an influencing factor in exocrine pancreatic function [22, 52]. There are theoretically 3 possible mechanisms leading to exocrine functional pancreatic disorder in patients suffering from pancreatic steatosis. These include:

(a) Lipotoxicity of acinar cells

(b) Adipocyte-mediated negative paracrine effect

(c) Direct destruction of acinar cells

Tahtaci et al. [53] published their results gained from a group of 43 patients suffering from pancreatic steatosis and a group of 48 persons without diagnosed pancreatic steatosis. These cohorts were examined by MRI, and the value of fecal elastase-1 was determined. Those persons suffering from diagnosed chronic pancreatitis, alcohol abuse, DM, celiac disease, inflammatory bowel disease, and those who had had surgical pancreatic intervention were excluded from this study. The authors found a significant reduction of fecal elastase-1 in patients with diagnosed pancreatic steatosis in comparison to those patients without steatosis. However, the authors found no differences in the relationship between NAFLD and the patients with or without diagnosed pancreatic steatosis. Therefore, the authors assumed, in contrast to the conclusions from, for example, d’Assignies et al. [54], that the relationship between NAFLD and NAFPD does not exist. This may be because NAFLD represents a different group among the patients with pancreatic steatosis.

Microbiome and NAFPD

We have not found any recently published work considering a relationship between a possible role of microbiome and NAFPD. However, there is a well-known described role between a gut microbiome and metabolic syndrome. In metabolic syndrome, a fat accumulation occurs in the pancreas, due to which there is also a relationship with NAFPD. Thus, the effect of a similar microbiome on the development of NAFPD can be assumed as in the metabolic syndrome [22, 55].

Chronic Pancreatitis

It’s clear that alcoholic steatosis of the pancreas can develop into chronic pancreatitis – probably due to chronic inflammation.

Acute pancreatitis or recurrent acute pancreatitis may lead to a reduction of the parenchymal mass and substitution with adipocytes. An increased number of pancreatic adipocytes can be observed in the pancreases of lean patients with nonhereditary/hereditary chronic pancreatitis [56].

That NAFPD progresses into chronic pancreatitis was not clearly described in the literature, but we know that recurrent acute pancreatitis is a risk factor for a chronic form of pancreatitis development. van Geenen et al. [57] found no relationship between pancreatic fibrosis and NAFPD. According to current evidence, fatty replacement and pancreatic fibrosis seem to both be independent consequences of chronic inflammation in patients with chronic pancreatitis [57].

NAFPD is a hot topic in gastroenterology. Just as obesity and metabolic syndrome are global problems, pancreatic steatosis especially in the form of NAFPD is an important challenge for pancreatologists, diabetologists, and nutritionists.

NAFPD should have consideration in clinical -practice. The evaluation of steatopancreatitis as early marker of ectopic fat accumulation and insulin resistance in persons with metabolic syndrome, as a prognostic marker for exocrine pancreatic insufficiency, chronic pancreatitis, and/or pancreatic cancer is important.

The growing incidence and prevalence of obesity, including metabolic syndrome, is a world health problem. Common risk factors for the development of NAFPD – as in older age, high body mass index, dyslipidemia, or metabolic syndrome with metabolic dysfunction – insulin resistance, are a real challenge for multidisciplinary research.

There is no doubt that systematic and extensive research as well as multicentric trials in these fields can be expected. The clinical consequences concerning NAFPD are not only numerous but also important from a practical standpoint. This is especially true if in our population >30% of the people are obese and about 30% have metabolic syndrome.

The authors declare that they have no ethical conflicts to disclose.

All authors declare no conflicts of interest in relation to this article.

No grants or financial support were provided.

Ogilvie R. The island of Langerhans in 19 cases of obesity.
J Pathol
. 1933;37(3):473–81.
Olsen TS. Lipomatosis of the pancreas in autopsy material and its relation to age and overweight.
Acta Pathol Microbiol Scand A
. 1978 Sep;86A(5):367–73.
Stamm BH. Incidence and diagnostic significance of minor pathologic changes in the adult pancreas at autopsy: a systematic study of 112 autopsies in patients without known pancreatic disease.
Hum Pathol
. 1984 Jul;15(7):677–83.
van Geenen EJ, Smits MM, Schreuder TC, van der Peet DL, Bloemena E, Mulder CJ. Nonalcoholic fatty liver disease is related to nonalcoholic fatty pancreas disease.
. 2010 Nov;39(8):1185–90.
Pezzilli R, Calculli L. Pancreatic steatosis: Is it related to either obesity or diabetes mellitus?
World J Diabetes
. 2014 Aug 15;5(4):415–9.
Smits MM, van Geenen EJ. The clinical significance of pancreatic steatosis.
Nat Rev Gastroenterol Hepatol
. 2011 Mar;8(3):169–77.
Tariq H, Nayudu S, Akella S, Glandt M, Chilimuri S. Non-alcoholic fatty pancreatic disease: A review of Literature.
Gastroenterol Res
. 2016 Dec;9(6):87–91.
Wang CY, Ou HY, Chen MF, Chang TC, Chang CJ. Enigmatic ectopic fat: prevalence of nonalcoholic fatty pancreas disease and its associated factors in a Chinese population.
J Am Heart Assoc
. 2014 Feb;3(1):e000297.
Lesmana CR, Pakasi LS, Inggriani S, Aidawati ML, Lesmana LA. Prevalence of Non-Alcoholic Fatty Pancreas Disease (NAFPD) and its risk factors among adult medical check-up patients in a private hospital: a large cross sectional study.
BMC Gastroenterol
. 2015 Dec;15(1):174.
Zhou J, Li ML, Zhang DD, Lin HY, Dai XH, Sun XL, et al. The correlation between pancreatic steatosis and metabolic syndrome in a Chinese population.
. 2016 Jul-Aug;16(4):578–83.
Pham YH, Bingham BA, Bell CS, Greenfield SA, John SD, Robinson LH, et al. Prevalence of pancreatic steatosis at a pediatric tertiary care center.
South Med J
. 2016 Mar;109(3):196–8.
Fraulob JC, Ogg-Diamantino R, Fernandes-Santos C, Aguila MB, Mandarim-de-Lacerda CA. A mouse model of metabolic syndrome: insulin resistance, fatty liver and non-alcoholic fatty pancreas disease (NAFPD) in C57BL/6 mice fed a high fat diet.
J Clin Biochem Nutr
. 2010 May;46(3):212–23.
Heni M, Machann J, Staiger H, Schwenzer NF, Peter A, Schick F, et al. Pancreatic fat is negatively associated with insulin secretion in individuals with impaired fasting glucose and/or impaired glucose tolerance: a nuclear magnetic resonance study.
Diabetes Metab Res Rev
. 2010 Mar;26(3):200–5.
Rossi AP, Fantin F, Zamboni GA, Mazzali G, Rinaldi CA, Del Giglio M, et al. Predictors of ectopic fat accumulation in liver and pancreas in obese men and women.
Obesity (Silver Spring)
. 2011 Sep;19(9):1747–54.
Carter R, Mouralidarane A, Soeda J, Ray S, Pombo J, Saraswati R, et al. Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms.
PLoS One
. 2014 Mar;9(3):e89505
Bojkova M, Dite P, Kunovsky L, Blaho M, -Kianicka B, Novotny I, et al. The role of -metabolic syndrome in induction of chronic pancreatitis after the first attack of acute pancreatitis – multicentric study. (In Press), Digestive Diseases.
Gaborit B, Abdesselam I, Kober F, Jacquier A, Ronsin O, Emungania O, et al. Ectopic fat storage in the pancreas using 1H-MRS: importance of diabetic status and modulation with bariatric surgery-induced weight loss.
Int J Obes
. 2015 Mar;39(3):480–7.
Jeong HT, Lee MS, Kim MJ. Quantitative analysis of pancreatic echogenicity on transabdominal sonography: correlations with metabolic syndrome.
J Clin Ultrasound
. 2015 Feb;43(2):98–108.
Sepe PS, Ohri A, Sanaka S, Berzin TM, Sekhon S, Bennett G, et al. A prospective evaluation of fatty pancreas by using EUS.
Gastrointest Endosc
. 2011 May;73(5):987–93.
Choi CW, Kim GH, Kang DH, Kim HW, Kim DU, Heo J, et al. Associated factors for a hyperechogenic pancreas on endoscopic ultrasound.
World J Gastroenterol
. 2010 Sep;16(34):4329–34.
Ustundag Y, Ceylan G, Hekimoglu K. Pancreatic hyperechogenicity on endoscopic ultrasound examination.
World J Gastroenterol
. 2011 Apr;17(15):2061–2.
Catanzaro R, Cuffari B, Italia A, Marotta F. Exploring the metabolic syndrome: nonalcoholic fatty pancreas disease.
World J Gastroenterol
. 2016 Sep;22(34):7660–75.
Kim SY, Kim H, Cho JY, Lim S, Cha K, Lee KH, et al. Quantitative assessment of pancreatic fat by using unenhanced CT: pathologic correlation and clinical implications.
. 2014 Apr;271(1):104–12.
Lee JS, Kim SH, Jun DW, Han JH, Jang EC, Park JY, et al. Clinical implications of fatty pancreas: correlations between fatty pancreas and metabolic syndrome.
World J Gastroenterol
. 2009 Apr;15(15):1869–75.
Saisho Y, Butler AE, Meier JJ, Monchamp T, Allen-Auerbach M, Rizza RA, et al. Pancreas volumes in humans from birth to age one hundred taking into account sex, obesity, and presence of type-2 diabetes.
Clin Anat
. 2007 Nov;20(8):933–42.
Hannukainen JC, Borra R, Linderborg K, Kallio H, Kiss J, Lepomäki V, et al. Liver and pancreatic fat content and metabolism in healthy monozygotic twins with discordant physical activity.
J Hepatol
. 2011 Mar;54(3):545–52.
Yu H, Shimakawa A, McKenzie CA, Brodsky E, Brittain JH, Reeder SB. Multiecho water-fat separation and simultaneous R2* estimation with multifrequency fat spectrum modeling.
Magn Reson Med
. 2008 Nov;60(5):1122–34.
Yokoo T, Shiehmorteza M, Hamilton G, Wolfson T, Schroeder ME, Middleton MS, et al. Estimation of hepatic proton-density fat fraction by using MR imaging at 3.0 T.
. 2011 Mar;258(3):749–59.
Popescu A, Săftoiu A. Can elastography replace fine needle aspiration?
Endosc Ultrasound
. 2014 Apr;3(2):109–17.
Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al.; International Diabetes Federation Task Force on Epidemiology and Prevention; Hational Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; International Association for the Study of Obesity. Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity.
. 2009 Oct;120(16):1640–5.
Abbasi F, Brown BW Jr, Lamendola C, McLaughlin T, Reaven GM. Relationship between obesity, insulin resistance, and coronary heart disease risk.
J Am Coll Cardiol
. 2002 Sep;40(5):937–43.
Côté M, Mauriège P, Bergeron J, Alméras N, Tremblay A, Lemieux I, et al. Adiponectinemia in visceral obesity: impact on glucose tolerance and plasma lipoprotein and lipid levels in men.
J Clin Endocrinol Metab
. 2005 Mar;90(3):1434–9.
Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease.
Circ Res
. 2005 May;96(9):939–49.
Kul S, Karadeniz A, Dursun İ, Şahin S, Faruk Çırakoğlu Ö, Raşit Sayın M, et al. el al. Non-alcoholic fatty pancreas disease is associated with increased epicardial adipose tissue and aortic intima-media thickness.
Acta Cardiol Sin
. 2019 Mar;35(2):118–25.
Bi Y, Wang JL, Li ML, Zhou J, Sun XL. The association between pancreas steatosis and metabolic syndrome: A systematic review and meta-analysis.
Diabetes Metab Res Rev
. 2019 Jul;35(5):e3142.
Della Corte C, Mosca A, Majo F, Lucidi V, Panera N, Giglioni E, et al. Nonalcoholic fatty pancreas disease and Nonalcoholic fatty liver disease: more than ectopic fat.
Clin Endocrinol (Oxf)
. 2015 Nov;83(5):656–62.
Wong VW, Wong GL, Yeung DK, Abrigo JM, Kong AP, Chan RS, et al. Fatty pancreas, insulin resistance, and β-cell function: a population study using fat-water magnetic resonance imaging.
Am J Gastroenterol
. 2014 Apr;109(4):589–97.
Lê KA, Ventura EE, Fisher JQ, Davis JN, Weigensberg MJ, Punyanitya M, et al. Ethnic differences in pancreatic fat accumulation and its relationship with other fat depots and inflammatory markers.
Diabetes Care
. 2011 Feb;34(2):485–90.
Chan JM, Rimm EB, Colditz GA, Stampfer MJ, Willett WC. Obesity, fat distribution, and weight gain as risk factors for clinical diabetes in men.
Diabetes Care
. 1994 Sep;17(9):961–9.
Ou HY, Wang CY, Yang YC, Chen MF, Chang CJ. The association between nonalcoholic fatty pancreas disease and diabetes.
PLoS One
. 2013 May;8(5):e62561.
Yu TY, Wang CY. Impact of non-alcoholic fatty pancreas disease on glucose metabolism.
J Diabetes Investig
. 2017 Nov;8(6):735–47.
Tushuizen ME, Bunck MC, Pouwels PJ, Bontemps S, van Waesberghe JH, Schindhelm RK, et al. Pancreatic fat content and beta-cell function in men with and without type 2 diabetes.
Diabetes Care
. 2007 Nov;30(11):2916–21.
van der Zijl NJ, Goossens GH, Moors CC, van Raalte DH, Muskiet MH, Pouwels PJ, et al. Ectopic fat storage in the pancreas, liver, and abdominal fat depots: impact on β-cell function in individuals with impaired glucose metabolism.
J Clin Endocrinol Metab
. 2011 Feb;96(2):459–67.
Stolzenberg-Solomon RZ, Adams K, Leitzmann M, Schairer C, Michaud DS, Hollenbeck A, et al. Adiposity, physical activity, and pancreatic cancer in the National Institutes of Health-AARP Diet and Health Cohort.
Am J Epidemiol
. 2008 Mar;167(5):586–97.
Michaud DS, Giovannucci E, Willett WC, Colditz GA, Stampfer MJ, Fuchs CS. Physical activity, obesity, height, and the risk of pancreatic cancer.
. 2001 Aug;286(8):921–9.
Tomita Y, Azuma K, Nonaka Y, Kamada Y, Tomoeda M, Kishida M, et al. Pancreatic fatty degeneration and fibrosis as predisposing factors for the development of pancreatic ductal adenocarcinoma.
. 2014 Oct;43(7):1032–41.
Lesmana CR, Gani RA, Lesmana LA. Non-alcoholic fatty pancreas disease as a risk factor for pancreatic cancer based on endoscopic ultrasound examination among pancreatic cancer patients: A single-center experience.
JGH Open
. 2017 Dec;2(1):4–7.
Tranchart H, Gaujoux S, Rebours V, Vullierme MP, Dokmak S, Levy P, et al. Preoperative CT scan helps to predict the occurrence of severe pancreatic fistula after pancreaticoduodenectomy.
Ann Surg
. 2012 Jul;256(1):139–45.
Gaujoux S, Torres J, Olson S, Winston C, Gonen M, Brennan MF, et al. Impact of obesity and body fat distribution on survival after pancreaticoduodenectomy for pancreatic adenocarcinoma.
Ann Surg Oncol
. 2012 Sep;19(9):2908–16.
Prachayakul V, Aswakul P. Pancreatic Steatosis: What Should Gastroenterologists Know? JOP.
J Pancreas (Online)
. 2015;16(3):227–31.
Miyake H, Sakagami J, Yasuda H, Sogame Y, Kato R, Suwa K, et al. Association of fatty pancreas with pancreatic endocrine and exocrine function.
PLoS One
. 2018 Dec;13(12):e0209448.
Pezzilli R, Andriulli A, Bassi C, Balzano G, Cantore M, Delle Fave G, et al.; Exocrine Pancreatic Insufficiency collaborative (EPIc) Group. Exocrine pancreatic insufficiency in adults: a shared position statement of the Italian Association for the Study of the Pancreas.
World J Gastroenterol
. 2013 Nov;19(44):7930–46.
Tahtacı M, Algın O, Karakan T, Yürekli ÖT, Alışık M, Köseoğlu H, et al. Can pancreatic steatosis affect exocrine functions of pancreas?
Turk J Gastroenterol
. 2018 Sep;29(5):588–94.
d’Assignies G, Ruel M, Khiat A, Lepanto L, Chagnon M, Kauffmann C, et al. Noninvasive quantitation of human liver steatosis using magnetic resonance and bioassay methods.
Eur Radiol
. 2009 Aug;19(8):2033–40.
Mishra AK, Dubey V, Ghosh AR. Obesity: an overview of possible role(s) of gut hormones, lipid sensing and gut microbiota.
. 2016 Jan;65(1):48–65.
Acharya C, Cline RA, Jaligama D, Noel P, Delany JP, Bae K, et al. Fibrosis reduces severity of acute-on-chronic pancreatitis in humans.
. 2013 Aug;145(2):466–75.
van Geenen EJ, Smits MM, Schreuder TC, van der Peet DL, Bloemena E, Mulder CJ. Smoking is related to pancreatic fibrosis in humans.
Am J Gastroenterol
. 2011 Jun;106(6):1161–6.
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.