The “fatty pancreas allograft”: anatomopathologic findings and clinical experience

Nghiem, Dai D.; Olson, Peter; Ormond, Debra

doi:10.1016/j.transproceed.2004.04.032

Cited by 20 publications

(15 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These findings are verified by histological reports of human pancreatic tissue that have clearly identified ectopic pancreatic fat as adipocyte infiltration visible between exocrine cells [11,15,41,42]. Additionally, whole-organ autopsies have reported that pancreatic fat consists only of patchy areas of intralobular or perilobular fat [15], or pancreatic fat dissecting islands of pancreatic tissue [41]; to date, no human autopsy has reported evidence of intracellular pancreatic fat and beta cell dysfunction caused by pancreatic steatosis [11,15,42]. Taken together, the present data provide evidence that the accumulation of triacylglycerols within pancreatic parenchymal tissue is not a major contributor to the development of type 2 diabetes.…”

Section: Discussionsupporting

confidence: 77%

“…Thus, results could also have been limited by the accuracy of the MRI method [16,38,46] for measuring low fat values or the method was not able to capture the irregular shape of the pancreas; higher pancreatic fat values could have reflected VAT infiltration. These findings are verified by histological reports of human pancreatic tissue that have clearly identified ectopic pancreatic fat as adipocyte infiltration visible between exocrine cells [11,15,41,42]. Additionally, whole-organ autopsies have reported that pancreatic fat consists only of patchy areas of intralobular or perilobular fat [15], or pancreatic fat dissecting islands of pancreatic tissue [41]; to date, no human autopsy has reported evidence of intracellular pancreatic fat and beta cell dysfunction caused by pancreatic steatosis [11,15,42].…”

Section: Discussionsupporting

confidence: 52%

“…However, the present comparison of 1 H-MRS techniques shows that non-invasive pancreatic fat measurements with localization via clinical T2-weighted images are not an accurate description of whole-organ fat, but are influenced by the inhomogeneous distribution of peripancreatic or interlobular fat that was visible in the highresolution mDIXON fat/water images [28]. While this inhomogeneous distribution of fat is in contrast to previous MRI reports [16,18], histological analyses of human pancreas tissue [11,15,41,42] confirm the inhomogeneous distribution of pancreatic adipose tissue infiltration found in this study. This inhomogeneous distribution of adipose tissue could also explain the discrepancies in 1 H-MRS [17,19,24] and MRI [16,18,21,38] pancreatic fat studies, and suggests that noninvasive methods that assess whole-organ adipose tissue infiltration [14,43] might provide more insight into the association between pancreas adipose tissue infiltration and beta cell function.…”

Section: Discussionmentioning

confidence: 56%

See 2 more Smart Citations

Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans

et al. 2015

View full text Add to dashboard Cite

Aims/hypothesis This study aimed to perform a comprehensive analysis of interlobular, intralobular and parenchymal pancreatic fat in order to assess their respective effects on beta cell function. Methods Fifty-six participants (normal glucose tolerance [NGT] (n=28), impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) (n=14) and patients with type 2 diabetes (n=14)) underwent a frequent-sampling OGTT and non-invasive magnetic resonance imaging (MRI; whole-body and pancreatic) and proton magnetic resonance spectroscopy ( 1 H-MRS; liver and pancreatic fat). Total pancreatic fat was assessed by a standard 2 cm H-MRS techniques revealed an inhomogeneous distribution of interlobular and intralobular adipose tissue, which increased with decreasing glucose tolerance. mDIXON-MRI measurements provided evidence against uniform steatosis, revealing regions of parenchymal tissue void of lipid accumulation in all participants. Total (r=0.385, p<0.01) and intralobular pancreas adipose tissue infiltration (r=0.310, p< 0.05) positively associated with age, but not with fasting or 2 h glucose levels, BMI or visceral fat content (all p>0.5). Furthermore, no associations were found between total and intralobular pancreatic adipose tissue infiltration and insulin secretion or beta cell function within NGT, IFG/IGT or patients with type 2 diabetes (all p>0.2). Conclusions/interpretation The pancreas does not appear to be another target organ for abnormal endocrine function because of ectopic parenchymal fat storage. No relationship was found between pancreatic adipose tissue infiltration and beta cell function, regardless of glucose tolerance status.

show abstract

Section: Discussionsupporting

confidence: 77%

Section: Discussionsupporting

confidence: 52%

Section: Discussionmentioning

confidence: 56%

See 1 more Smart Citation

Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Some researchers insist that steatosis in the pancreas or fat deposition in pancreatic cells does not exist in humans [12] . However, according to some studies that contained pathological observations on the human pancreas [3][4][5] , fat deposition in the human pancreas appears to occur mainly in interlobular septa, rather than in cells. However, it is difficult to arrive at clear conclusions due to the difficulty of tissue collection from the pancreas, which limits histological proof.…”

Section: Discussionmentioning

confidence: 99%

“…However, another study reported that there was no histological evidence of the existence of steatosis in the human pancreas and no reports have clearly demonstrated that the increase of pancreas echogenicity implied steatosis of the pancreas or fat deposition [2] . Autopsy studies reported pathologic findings of pancreatic steatosis in interlobular septa rather than in pancreas acinar cells [3][4][5] , and fat deposition related to aging [6,7] . According to an animal study, pancreatic steatosis caused anomalies of pancreas islet cells leading to hyperglycemia [8][9][10] .…”

Section: Introductionmentioning

confidence: 99%

Clinical implications of fatty pancreas: Correlations between fatty pancreas and metabolic syndrome

Lee¹,

Kim²,

Jun³

et al. 2009

WJG

249

277

View full text Add to dashboard Cite

AIM:To investigate the clinical implications of lipid deposition in the pancreas (fatty pancreas). METHODS:The subjects of this study were 293 patients who had undergone abdominal computed tomography (CT) and sonography. Fatty pancreas was diagnosed by sonographic findings and subdivided into mild, moderate, and severe fatty pancreas groups comparing to the retroperitoneal fat echogenicity. RESULTS:Fatty pancreas was associated with higher levels for visceral fat, waist circumference, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol, triglyceride, high density lipoprotein, free fatty acid, γ-GTP, insulin, and the homeostasis model assessment of insulin resistance (HOMA-IR) than the control group (P < 0.05). HOMA-IR, visceral fat, triglyceride, and ALT also tended to increase with the degree of fat deposition in the pancreas on sonography. In a multivariate logistic regression analysis, HOMA-IR, visceral fat, and ALT level were independently related to fatty pancreas after adjustment for age, body mass index, and lipid profile. The incidence of metabolic syndrome in the fatty pancreas group was significantly higher than in the control group, and the numbers of metabolic syndrome parameters were significantly higher in the fatty pancreas group (P < 0.05).CONCLUSION: Sonographic fatty pancrease showed higher insulin resistance, visceral fat area, triglyceride, and ALT levels than normal pancreases. Fatty pancreas also showed a strong correlation with metabolic syndrome.

show abstract

Type 2 diabetes: Does pancreatic fat really matter?

Guglielmi

Sbraccia

2017

Diabetes Metabolism Res

View full text Add to dashboard Cite

SummaryWith the increasing prevalence of obesity, the interest of research in nonalcoholic fatty pancreas disease (NAFPD) has grown. Even though the pancreas appears more susceptible to lipid accumulation compared with the liver, NAFPD has been less investigated due to the limits in detecting techniques. Several definitions and synonyms for NAFPD are used by authors and can be misleading. This, together with differences in methodology and ethnicity, make the integration and comparison of studies on this topic challenging. NAFPD could be used as an early indicator of ectopic fat deposition, which is recognized as a key factor of obesity cardio-metabolic complications. However, evidence that NAFPD has a pathogenetic role in type 2 diabetes is also emerging. This article reviews the current state of knowledge on the clinical and pathophysiologic relevance of NAFPD in β-cell function and insulin resistance.KEYWORDS ectopic fat depots, nonalcoholic fatty liver disease, pancreatic fat, pancreatic steatosis, type 2 diabetes, β-cell dysfunction | INTRODUCTIONThe global epidemic of obesity may largely explain the concurrent increase in the incidence and prevalence of type 2 diabetes (T2DM) over the last decades.Therefore, the study of adipose tissue biology has gained an enormous research interest. This has gradually transformed adipose tissue from an inert lipid store into a metabolically dynamic endocrine organ capable of synthesizing biologically active compounds involved in metabolic homeostasis, as well as in many biological functions. [1][2][3] Although the epidemiological association between obesity and T2DM in general is well described, 4 the evidence of pathophysiological connection between them has been fully appreciated only in recent years. This issue has raised even more attention because of accumulating evidence that also a modest weight loss, induced by dietary interventions, 5,6 physical exercise, 7,8 and drugs and bariatric surgery procedures, 9,10 is capable of significantly reducing T2DM risk and improving glycemic control. | THE CAUSAL LINK BETWEEN OBESITY AND TYPE DIABETESGenome-wide association scans (GWAS) and candidate gene approaches have so far identified ∼40 genes associated with T2DM and a similar number, but different, with obesity. 11,12 Most of T2DM genes appear related to β-cell dysfunction, with many fewer involved in pathways related to insulin resistance independent of adiposity. 13 However, the identified genes are estimated to predict only 15% of T2DM. 14 This low predictive power may reflect the importance of environmental factors and epigenetic or gene-environment interactions that are not detected by population genetics-based methods. Initially, insulin resistance can be overcome by an increased insulin production by the pancreas, resulting in hyperinsulinemia. Afterwards, during the progression towards overt T2DM, β-cell failure to compensate adequately the greater insulin requirements occurs. [18][19][20] The common dysfunctional β-cell phenotype in T2DM is characterized by dimi...

show abstract

The “fatty pancreas allograft”: anatomopathologic findings and clinical experience

Cited by 20 publications

References 2 publications

Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans

Pancreatic adipose tissue infiltration, parenchymal steatosis and beta cell function in humans

Clinical implications of fatty pancreas: Correlations between fatty pancreas and metabolic syndrome

Type 2 diabetes: Does pancreatic fat really matter?

Contact Info

Product

Resources

About