Nonalcoholic Fatty Pancreas Disease Research Articles

Predictive value of anthropometric and biochemical indices in non-alcoholic fatty pancreas disease: a cross-sectional study

ObjectivesTriglyceride (TG), triglyceride-glucose index (TyG), body mass index (BMI), TyG-BMI and triglyceride to high-density lipoprotein ratio (TG/HDL) have been reported to be reliable predictors of non-alcoholic fatty liver disease. However,...

Western diet-induced ultrastructural changes in mouse pancreatic acinar cells.

Mouse models of diet-induced type 2 diabetes mellitus provide powerful tools for studying the structural and physiological changes that are related to the disease progression. In this study, diabetic-like glucose dysregulation was induced in mice by feeding them a western diet, and light and transmission electron microscopy were used to study the ultrastructural changes in the pancreatic acinar cells. Acinar necrosis and vacuolization of the cytoplasm were the most prominent features. Furthermore, we observed intracellular and extracellular accumulation of lipid compounds in the form of lipid droplets, structural enlargement of the cisternae of the rough endoplasmic reticulum (RER), and altered mitochondrial morphology, with mitochondria lacking the typical organization of the inner membrane. Last, autophagic structures, i.e., autophagosomes, autolysosomes, and residual bodies, were abundant within the acinar cells of western diet-fed mice, and the autolysosomes contained lipids and material of varying electron density. While diets inducing obesity and type 2 diabetes are clearly associated with structural changes and dysfunction of the endocrine pancreas, we here demonstrate the strong effect of dietary intervention on the structure of acinar cells in the exocrine part of the organ before detectable changes in plasma amylase activity, which may help us better understand the development of non-alcoholic fatty pancreas disease and its association with endo- and exocrine dysfunction.

Reduced Branched-Chain Amino Acid Intake Improved High-Fat Diet-Induced Nonalcoholic Fatty Pancreas Disease in Mice.

To explore the effects of branched-chain amino acids (BCAAs) on nonalcoholic fatty pancreas disease (NAFPD) and its possible mechanism in high-fat diet (HFD) induced mice. Pancreatic morphology and lipid infiltration was assessed by hematoxylin-eosin staining and immunohistochemistry, and lipid levels in the pancreas were determined using colorimetric enzymatic method. Relevant mechanism was investigated using western blotting and biochemical test. In HFD-fed mice, dietary BCAAs restriction could attenuate body weight increase, improve glucose metabolism, and reduce excessive lipid accumulation in the pancreas. Furthermore, expression of AMPKα and downstream uncoupling protein 1 were upregulated, while genes related to mammalian target of rapamycin complex 1 (mTORC1) signal pathway and lipid de novo synthesis were suppressed in HFD-BCAA restriction group compared with HFD and HFD-high BCAAs fed mice. In addition, BCAA restriction upregulated expression of BCAAs related metabolic enzymes including PPM1K and BCKDHA, and decreased the levels of BCAAs and branched chain keto acid in the pancreas. However, there was no difference in levels of lipid content in the pancreas and gene expression of AMPKα and mTORC1 between HFD and HFD-high BCAAs groups. Branched-chain amino acid restriction ameliorated HFD-induced NAFPD in mice by activation of AMPKα pathway and suppression of mTORC1 pathway.

Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease.

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.

Non-alcoholic Fatty Pancreas Disease (NAFPD): An updated review

Ectopic accumulation of fat can cause a variety of metabolic diseases, and the emerging non-alcoholic fatty pancreas disease (NAFPD) is increasingly being recognized by clinicians as a cause for concern. NAFPD is a disease caused by abnormal accumulation of adipose tissue in the pancreas, which is related to obesity. The main feature of NAFPD is death of acinar cells, which are then replaced by adipose cells. However, the underlying molecular mechanisms have not been fully explored. Obesity, aging, and metabolic syndrome are independent risk factors for the occurrence and development of NAFPD. Studies have shown that NAFPD leads to insulin resistance and pancreatic dysfunction, increases the risk of diabetes, worsens the severity of pancreatitis, and is significantly correlated with pancreatic cancer and postoperative pancreatic fistula. There is no standard treatment for NAFPD; exercise, a balanced diet, and lifestyle can help reduce pancreatic fat; however, other treatment modalities such as drugs and bariatric surgery are still being explored. The specific pathological mechanism of NAFPD remains unclear, and its potential association with various clinical diseases requires further study. This review summarizes the etiology, diagnosis, clinical consequences, and potential therapeutic strategies of NAFPD.

Nonalcoholic Fatty Pancreas Disease

Nonalcoholic fatty pancreas disease (NAFPD) is a condition characterized by the accumulation of excess fat in the pancreas, commonly occurring in individuals with obesity. The diagnostic evaluation of NAFPD is mostly composed of image tests, but it is still less standardized. NAFPD is closely linked to metabolic syndrome, type 2 diabetes, pancreatic exocrine insufficiency, acute pancreatitis, pancreatic fistula, pancreatic cancer, and nonalcoholic fatty liver disease (NAFLD). However, further research is needed to investigate the mechanisms underlying these relevant clinical consequences. In terms of treatment, strategies aimed at minimizing pancreatic fat accumulation through dietary modifications and regular exercise, similar to the management of NAFLD, may be beneficial.

Evaluation of Development of Nonalcoholic Fatty Pancreas Disease After Post-Endoscopic Retrograde Cholangiop ancreatography Pancreatitis in Liver Transplant Patients: Computerized Tomography Versus Ultrasound.

Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common serious adverse event in liver transplant patients The average incidence has been reported as 1.3%-15.1% in prospective series. In our study, we have prospectively evaluated the prevalence of nonalcoholic fatty pancreatic disease (NAFPD) after PEP via computerized tomography (CT) and determined the ratio of fatty pancreas by ultrasound imaging in liver transplant patients. We have retrospectively analyzed 2922 patient files, and 146 patients were indicated for ERCP. PEP was observed in 32 patients. After presenting the significant association between the NAFPD and PEP, we prospectively reached 32 patients included in the study. Ten out of those patients have been performed ultrasound with regard to NAFPD. PEP was defined in 32 patients in whom CT was performed to investigate NAFPD. When the patients were contacted, it was observed that 12% were deceased, 71% were alive, but 15% of them were untraceable. Ultrasound has been performed on 10 of 32 patients to determine NAFPD. There was a significant reduction in post-PEP pancreas/spleen rate compared to pre-PEP pancreas/ spleen rate (P = .001). Both the pre-PEP and post-PEP pancreas-spleen difference dropped significantly (P = .002). Ultrasound imaging could be utilized as a scanning test and an alternative to evaluate and diagnose NAFPD, particularly in risky patients.

S57 The Prevalence and Association Between Non-Alcoholic Fatty Pancreas Disease and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis

S57 The Prevalence and Association Between Non-Alcoholic Fatty Pancreas Disease and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis

Hypothyroidism and subclinical hypothyroidism are associated with fatty pancreas (Non-Alcoholic Fatty Pancreas Disease).

Increasing visceral fat deposition with raised prevalence of obesity and metabolic syndrome is associated with many adverse conditions, especially cardiovascular diseases and diabetes. Although there are many studies that investigate hepatic steatosis in hypothyroidism and subclinical hypothyroidism, to the best of our knowledge, there is no study investigating its relationship with pancreatic steatosis. In the present study, the purpose was to investigate this relationship. Physical and biochemical characteristics of 30 hypothyroid, 30 subclinical hypothyroid, and 30 euthyroid volunteers were recorded in this cross-sectional study. Liver and pancreatic steatosis were evaluated with ultrasonography. It was found that pancreatic steatosis was increased in hypothyroid and subclinical groups when compared to the control group, and hepatic steatosis was increased in the subclinical group when compared to the control group (steatosis; p=0.002, p=0.004, p=0.001, p=0.002, p=0.002, p=0.004). Pancreatic steatosis was positively correlated with age, hepatic steatosis, height, weight, BMI, waist circumference, hip circumference, hemoglobin, Insulin, alanine aminotransferase, Triglyceride, Creatinine, and gamma-glutamyltransferase and was negatively correlated with total cholesterol, high-density lipoproteins. The prevalence of pancreatic steatosis was found to be increased in hypothyroidism and subclinical hypothyroidism when compared with the euthyroid control group.

Non-alcoholic fatty pancreas disease and pancreatic exocrine insufficiency: pilot study and systematic review

Introduction 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 and methods 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. Results 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. Conclusion 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.

Non-Alcoholic Fatty Pancreas Disease: The Unsung Disease.

Non-alcoholic fatty pancreas disease (NAFPD) is a relatively new and emerging disease that is increasingly diagnosed yearly, like non-alcoholic fatty liver disease (NAFLD). It is associated especially with metabolic syndrome and obesity. As awareness of pancreatic steatosis and its clinical implications increase, it is diagnosed more frequently. The researchers have explained the clinical importance of NAFPD and the diseases it causes, such as pancreatitis, pancreatic insufficiency, and pancreatic cancer. Although the definitive treatment is not yet established, the primary treatment approach is weight loss since NAFPD is associated with metabolic syndrome as well as obesity. Although pharmacological agents, such as oral hypoglycemic agents, have been investigated in animal experiments, studies on humans have not been conducted. Since the research on NAFPD is still insufficient, it is a subject that needs to be investigated, and further studies are needed to explore its pathophysiology, clinical impact, and its management.

IS FATTY PANCREAS LINKED TO METABOLIC SYNDROME ?

AIM : The study aimed to nd the link between the fat deposition in pancreas and liver and metabolic syndrome. METHODOLOGY : It was a cross sectional study . 50 patients with ultrasonographic evidence of fatty pancreas were included and were evaluated for the presence of fatty liver on ultrasonography and were assessed for the presence of metabolic syndrome. RESULTS: Metabolic syndrome was detected in 62% of patients of Non alcoholic fatty pancreas disease (NAFPD). The overall prevalence of fatty liver was 72% in patients with NAFPD. The presence of fatty liver in the studied patients increased the number of parameters of metabolic syndrome. It was statistically signicant (p=0.043). CONCLUSION: NAFPD is closely related to metabolic syndrome and fatty liver

Automated image analysis method to detect and quantify fat cell infiltration in hematoxylin and eosin stained human pancreas histology images

Fatty infiltration in pancreas leading to steatosis is a major risk factor in pancreas transplantation. Hematoxylin and eosin (H and E) is one of the common histological staining techniques that provides information on the tissue cytoarchitecture. Adipose (fat) cells accumulation in pancreas has been shown to impact beta cell survival, its endocrine function and pancreatic steatosis and can cause non-alcoholic fatty pancreas disease (NAFPD). The current automated tools (E.g. Adiposoft) available for fat analysis are suited for white fat tissue which is homogeneous and easier to segment unlike heterogeneous tissues such as pancreas where fat cells continue to play critical physiopathological functions. The currently, available pancreas segmentation tool focuses on endocrine islet segmentation based on cell nuclei detection for diagnosis of pancreatic cancer. In the current study, we present a fat quantifying tool, Fatquant, which identifies fat cells in heterogeneous H and E tissue sections with reference to diameter of fat cell. Using histological images from a public database, we observed an intersection over union of 0.797 to 0.962 and 0.675 to 0.937 for manual versus Fatquant analysis of pancreas and liver, respectively.

Non-Alcoholic Fatty Liver and Fatty Pancreas Diseases Associate with Acute Pancreatitis

Objective: Fat accumulation in the liver and pancreas are clinical manifestations of metabolic syndrome and associated with inflammation. It was 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.&#x0D; Patients and methods: This retrospective and cross sectional study was consisted of 194 participants who admitted to the hospital with an abdominal pain complaint and undergone 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 liver and pancreas were determined according to abdominal CT.&#x0D; Results: A statistical significance was observed for the development of acute pancreatitis when patients with normoglycemia were compared to both 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 was revealed that prediabetes, type 2 diabetes, NAFLD and NAFPD according to median value were risk factors for the acute pancreatitis (p

Effects of Lactoferrin Supplemented with Fermented Milk on Obesity-Associated Pancreatic Damage in Rats.

Non-alcoholic fatty pancreas disease is a newly emerging disease that represents an important risk factor for the development of pancreatic cancer. Obesity is a risk factor for pancreatic diseases, including pancreatitis and pancreatic cancer. On the other hand, the development of healthy aspects-based food products is a recent trend. Lactoferrin is a component of the body's immune system, which interacts with DNA, RNA, polysaccharides, and heparin, and it has many biological functions and many important immunomodulatory properties. Thus, this study aims to investigate the enhancement effect of supplementation of lactoferrin with stirred yogurt on weight gain, lipid profile, glucose level, and pancreatic enzymes in animals fed a high-fat diet (HFD). Forty-eight female albino rats were divided into 6 groups treated orally for 45 days as follows: negative control (basal diet), positive control (add 1% cholesterol), stirred yogurt (SY), Lactoferrin LF (100 mg/kg bw), supplementation of lactoferrin with stirred yogurt SY-LF at two concentrations LF1 (50 mg/kg bw) and LF2 (100 mg/kg bw). Blood and pancreas samples were collected for different analyses. Animals fed with a HFD showed a significant increase in body weight, total cholesterol, triglyceride, low-density lipoprotein (LDL), glucose level, amylase, and Lipase enzymes (44.72%, 151.33 mg/dL, 142.67 mg/dL, 85.37 mg/dL, 141.33 mg/dL, 39.33 U/mL, 23.43 U/mL). Moreover, it observed a significant decrease in high-density lipoprotein (HDL, 37.33 mg/dL); meanwhile, SY fortified with lactoferrin was useful in losing weight gain and improving lipid profile, pancreas function, and histological change in the pancreas. The supplementation of lactoferrin at 100 mg/Kg bw with LB. Acidophilus as a probiotic was more effective for pancreas functions. This application is a natural protective alternative to manufactured medicines for children and the elderly as a natural product.

Relation Between Non-Alcoholic Fatty Pancreas and Clinical and Biochemical Parameters in Women with Polycystic Ovary Syndrome: A Multi-Centric Study.

Polycystic ovary syndrome (PCOS) is the most common endocrinological disease affecting women in the reproductive age. Non-alcoholic fatty pancreas disease (NAFPD) can promote many aspects of pancreatic dysfunction. The present study aimed to determine the prevalence of NAFPD and to identify its association with clinical and biochemical parameters in PCOS patients. The present study included 150 patients with PCOS and 150 age-matched healthy controls. All patients were submitted to careful history taking and thorough clinical examination. Performed laboratory investigations included fasting and postprandial blood glucose, lipid profile, liver function tests, serum prolactin and total testosterone. Fatty pancreas was diagnosed using abdominal ultrasound. Among PCOS women, NAFPD was diagnosed in 57 women (38.0%) in contrast to 18 women (12.0%) in the control group (p < 0.001). Patients with NAFPD were significantly older [median (IQR): 38.0 (35.0-43.0) versus 29.0 (25.5-33.0) years, p = 0.001] with higher BMI [median (IQR): 31.5 (29.1-34.7) versus 30.4 (28.6-32.4) kg/m2, 0.042]. Moreover, they had significantly higher frequency of metabolic syndrome (84.2% versus 54.8%, p = 0.001), insulin resistance (68.4% versus 26.9%, p < 0.001) and severe NAFLD (22.8% versus 2.2%, p < 0.001). NAFPD patients had significantly lower sex hormone binding globulin (SHBG) [median (IQR): 36.0 (30.8-40.7) versus 38.1 (35.15-42.7), p = 0.002] and significantly higher free androgen index (FAI) [median (IQR): 4.08 (3.3-4.92) versus 3.47 (3.12-4.05), p < 0.001]. NAFPD is prevalent PCOS. It is related to metabolic syndrome, insulin resistance, dyslipidemia and hyperandrogenism.

Non-Alcoholic Fatty Pancreas Disease is Associated with SYNTAX Score in Acute Coronary Syndrome.

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. 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. 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. 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. 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.

Lipid accumulation in the pancreas: clinical significance of NAFPD (non-alcoholic fatty pancreas disease)

Pancreatic lipid accumulation - which is known as NAFPD (non-alcoholic fatty pancreas disease) - has gained an increasing attention in the last couple of years. Previously, this alteration was mentioned using different names. Undoubtedly, the term of NAFPD is still rarely used in the Hungarian scientific literature, even the proper translation should be considered difficult. Pancreatic lipid accumulation is a clinical manifestation of ectopic occurrence of adipose tissue. NAFPD can be diagnosed by different imaging modalities. Although proper quantification of pancreatic lipid accumulation is challenging, ultrasonography and computed tomography are used in clinical practice. The prevalence of NAFPD was about 30-35% in different adult populations but a relatively higher frequency might also be observed in children and adolescents with obesity. NAFPD may influence both endocrine and exocrine functions of the pancreas. Clinical studies documented a close correlation between NAFPD and type 2 diabetes/metabolic syndrome. Local consequences of pancreatic lipid accumulation are less recognized but clinical observations suggested that NAFPD might play a role in the development of acute and chronic pancreatitis, pancreatic cancer, and pancreatic exocrine dysfunction. Therapeutically, weight loss in patients with obesity, due to life-style modification, pharmacological intervention or bariatric surgery, may reduce pancreatic lipid accumulation. Importantly, antihyperglycemic treatment of patients with type 2 diabetes should be performed by using antidiabetic drugs providing not only proper glycaemic control but even weight loss. NAFPD is a relatively new clinical entity which is rather common and probably underdiagnosed. Basic and new data about NAFPD are of importance for clinicians working in the field of different specialties and sub-specialties (internal medicine, gastroenterology, diabetology, lipidology, obesitology, surgery). Orv Hetil. 2022; 163(44): 1735-1742.

The Endocrine–Metabolic Axis Regulation in Offspring Exposed to Maternal Obesity—Cause or Consequence in Metabolic Disease Programming?

Obesity incidence is rising worldwide, including women of reproductive age, contributing to increased gestations in which Maternal Obesity (MO) occurs. Offspring born to obese mothers present an increased predisposition to develop metabolic (e.g., obesity, diabetes) and cardiovascular disease (CVD). The developmental programming of the metabolic dysfunction in MO offspring can initiate in utero. The different availability of metabolic substrates, namely glucose, can modulate cellular growth, proliferation, and differentiation, resulting in different levels of tissue maturation and function. We defined the remodelling of these early processes as the first hit of metabolic disease programming. Among these, adipocyte early differentiation and gut dysbiosis are initial repercussions occurring in MO offspring, contributing to -tissue-specific dysfunction. The second hit of disease programming can be related to the endocrine–metabolic axis dysregulation. The endocrine–metabolic axis consists of multi-organ communication through the release of factors that are able to regulate the metabolic fate of cells of organs involved in physiological metabolic homeostasis. Upon adipose tissue and gut early dysregulation, these organs’ endocrine function can be programmed to the disrupted release of multiple factors (e.g., adiponectin, leptin, glucagon-like peptide). This can be perceived as a natural mechanism to overcome metabolic frailty in an attempt to prevent or postpone organ-specific disease. However, the action of these hormones on other tissues may potentiate metabolic dysfunction or even trigger disease in organs (liver, pancreas, heart) that were also programmed in utero for early disease. A second phase of the endocrine–metabolic dysregulation happens when the affected organs (e.g., liver and pancreas) self-produce an endocrine response, affecting all of the involved tissues and resulting in a new balance of the endocrine–metabolic axis. Altogether, the second hit exacerbates the organ-specific susceptibility to disease due to the new metabolic environment. The developmental programming of the endocrine–metabolic axis can start a vicious cycle of metabolic adaptations due to the release of factors, leading to an endocrine response that can jeopardize the organism’s function. Diseases programmed by MO can be boosted by endocrine dysregulation, namely Non-Alcoholic Fatty Liver Disease, Non-Alcoholic Fatty Pancreas Disease, and the aggravation of the adipose tissue and gut dysfunction. Chronic metabolic dysregulation can also predispose MO offspring to CVD through the modulation of the endocrine environment and/or the metabolic status. To cease the vicious cycle of MO disease transmission among generations and-provide preventive and specialized prenatal and postnatal care to MO offspring, it is necessary to understand the molecular mechanisms underlying the MO-related disease development. In this review, we summarize most of the developmental programming molecular events of the endocrine–metabolic axis described on the offspring exposed to MO, providing a brief overview of the potential mechanisms that predispose MO offspring to metabolic disease, and discuss the programming of the endocrine–metabolic axis as a plausible mechanism for metabolic disease predisposition in MO offspring.

The association of non-alcoholic fatty pancreas disease and glycemic status

Background: Non-alcoholic fatty pancreas disease (NAFPD) is an emerging clinical entity. NAFPD is characterised by excessive fat deposition in the pancreas in the absence of alcohol consumption. Recent studies suggest that NAFPD might be associated with beta cell dysfunction, insulin resistance and inflammation which might lead to development of diabetes. NAFPD might be used as an initial indicator of glucometabolic disturbances and identify the patients with prediabetes.Methods: This was a cross sectional study in which the glycemic status of 50 patients with NAFPD with ultrasonographic evidence of increased echogenicity of pancreas was assessed and association between glycemic variability and NAFPD was determined. The patients were also assessed for the ultrasonographic evidence of fatty liver.Results: Pre-diabetes was noted in 32% subjects while diabetes was noted in 20% subjects. Thus, 52% patients with NAFPD had abnormal glycemic status. The 48% subjects i.e., 24 patients had normoglycemia. The presence of fatty liver was statistically significant in normoglycemia and diabetes mellitus with p=0.001 and 0.045 respectively. No statistically significant association was noted between fatty liver and prediabetes with p=0.175. No causal relationship was seen between fatty liver and glycemic variability in patients with NAFPD.Conclusions: NAFPD is associated with impaired glycemic status. It is also seen frequently with fatty liver. Its early detection may help to identify the patients with prediabetes who may benefit from timely introduction of interventions to reduce the rising morbidity and mortality due to diabetes mellitus.