Intra-pancreatic fat deposition: bringing hidden fat to the fore

Author(s):  
Maxim S. Petrov ◽  
Roy Taylor
Author(s):  
Juyeon Ko ◽  
Loren Skudder-Hill ◽  
Conor Tarrant ◽  
Wandia Kimita ◽  
Sakina H. Bharmal ◽  
...  

Diseases ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 25
Author(s):  
Andre E. Modesto ◽  
Juyeon Ko ◽  
Charlotte E. Stuart ◽  
Sakina H. Bharmal ◽  
Jaelim Cho ◽  
...  

Background: Skeletal muscle has been implicated in the pathogenesis of type 2 diabetes but it has never been investigated in diabetes after pancreatitis. The aim was to investigate the relationship between psoas muscle volume (PMV) and diabetes in individuals after pancreatitis, as well as its associations with ectopic fat phenotypes and insulin traits. Methods: Individuals after an attack of pancreatitis and healthy individuals were studied in a cross-sectional fashion. All participants underwent magnetic resonance imaging, based on which PMV, skeletal muscle fat deposition (SMFD), as well as liver and intra-pancreatic fat depositions were derived. Fasting and postprandial blood samples were collected to calculate indices of insulin sensitivity and secretion. Linear regression analyses were conducted, adjusting for possible confounders (age, sex, body composition, comorbidities, use of insulin, and others). Results: A total of 153 participants were studied. PMV was significantly decreased in the diabetes group compared with healthy controls (β = −30.0, p = 0.034 in the most adjusted model). SMFD was significantly inversely associated with PMV (β = −3.1, p < 0.001 in the most adjusted model). The Matsuda index of insulin sensitivity was significantly directly associated with PMV (β = 1.6, p = 0.010 in the most adjusted model). Conclusions: Diabetes in individuals after pancreatitis is characterized by reduced PMV. Reduced PMV is associated with increased SMFD and decreased insulin sensitivity in individuals after pancreatitis.


2020 ◽  
Vol 8 (1) ◽  
pp. e001508 ◽  
Author(s):  
Tomomi Horii ◽  
Yukari Fujita ◽  
Chisaki Ishibashi ◽  
Kenji Fukui ◽  
Hidetoshi Eguchi ◽  
...  

IntroductionChronic inflammation is observed in type 2 diabetes islets, and fat deposition in the pancreas affects insulin secretion and glucose tolerance. However, the relationship between this inflammation and pancreatic fat deposition has not been elucidated.Research design and methodsWe examined pancreatic sections from 60 Japanese patients obtained by pancreatectomy. We evaluated pancreatic fat-cell area (%) and CD68-positive (CD68+) cells per islet histologically and examined the relationships between these histological findings and various clinical parameters.ResultsThe number of CD68+ cells per islet in the diabetes group was significantly higher than that in the normal glucose tolerance group (p=0.026). Moreover, CD68+ cells per islet were significantly correlated with body mass index (r=0.33, p=0.0080), fasting C-peptide immunoreactivity (r=0.46, p=0.0042), homeostasis model assessment insulin resistance (r=0.38, p=0.016), C-peptide index (r=0.38, p=0.018), the area under the glucose concentration curve (AUCglucose) at the 75 g oral glucose tolerance test (r=0.49, p=0.0065) and fat-cell area (r=0.51, p<0.0001). In multiple regression analyses, fat-cell area (β=0.600, p=0.0027) and AUCglucose (β=0.453, p=0.0042) were the independent and significant determinants of CD68+ cells per islet.ConclusionThe inflammation of islets is associated with pancreatic fatty infiltration and hyperglycemia, which may further aggravate glucose tolerance.


Pancreatology ◽  
2018 ◽  
Vol 18 (4) ◽  
pp. 429-437 ◽  
Author(s):  
Peter O. Coe ◽  
Steve R. Williams ◽  
David M. Morris ◽  
Ed Parkin ◽  
Michelle Harvie ◽  
...  

2019 ◽  
Vol 24 (11) ◽  
pp. 2560-2569 ◽  
Author(s):  
Uma L. Sreedhar ◽  
Steve V. DeSouza ◽  
Brittany Park ◽  
Maxim S. Petrov

Cytokine ◽  
2019 ◽  
Vol 120 ◽  
pp. 107-114 ◽  
Author(s):  
Ruma G. Singh ◽  
Ngoc Nhu Nguyen ◽  
Aya Cervantes ◽  
Gisselle C. Alarcon Ramos ◽  
Jaelim Cho ◽  
...  

Obesity Facts ◽  
2021 ◽  
pp. 1-13
Author(s):  
Juyeon Ko ◽  
Loren Skudder-Hill ◽  
Sunitha Priya ◽  
Wandia Kimita ◽  
Sakina H. Bharmal ◽  
...  

<b><i>Introduction:</i></b> Ectopic fat deposition in the pancreas is involved in the pathogenesis of metabolic sequelae following an attack of pancreatitis. However, its relationship with the exocrine pancreas has never been explored in this setting. The aim was to investigate the associations between intra-pancreatic fat deposition (IPFD), pancreas size, and pancreatic enzymes. <b><i>Methods:</i></b> This cross-sectional study recruited individuals with a history of acute pancreatitis and healthy controls. All participants underwent 3T magnetic resonance imaging, from which IPFD, total pancreas volume (TPV), and pancreas diameters (across the head, body, and tail) were measured independently by 2 raters in a blinded fashion. Circulating levels of pancreatic amylase, pancreatic lipase, and chymotrypsin were measured in a fasted state. A series of linear regression analyses was conducted, accounting for possible confounders. <b><i>Results:</i></b> A total of 108 individuals with pancreatitis and 60 healthy controls were studied. There was a statistically significant difference in IPFD (<i>p</i> &#x3c; 0.001), but not in TPV (<i>p</i> = 0.389), between the groups. In the post-pancreatitis group, IPFD was significantly inversely associated with pancreas tail diameter (β = −0.736, <i>p</i> = 0.036 in the most adjusted model). In the control group, IPFD was significantly inversely associated with TPV (β = −3.557, <i>p</i> = 0.026 in the most adjusted model). Levels of pancreatic amylase were significantly directly associated with pancreas tail diameter in the post-pancreatitis group (β = 3.891, <i>p</i> = 0.042 in the most adjusted model), whereas levels of pancreatic lipase were significantly inversely associated with TPV in the control group (β = −10.533, <i>p</i> = 0.024 in the most adjusted model). <b><i>Conclusion:</i></b> Increased IPFD in individuals after an attack of pancreatitis is associated with reduced pancreas tail diameter, which is in turn associated with reduced circulating levels of pancreatic amylase. The relationship between IPFD and the exocrine pancreas warrants further investigations.


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