Pancreas Fat Content Research Articles

Abdominal magnetic resonance imaging assessment and quantification of pancreatic and liver adipose tissues in obesity before and after laparoscopic sleeve gastrectomy

ObjectivesTo investigate the changes of liver and pancreas fat fraction after laparoscopic sleeve gastrectomy (LSG) by magnetic resonance imaging (MRI). MethodsOur study included morbid obesity with normal blood glucose and underwent abdominal MRI before and after LSG. In total, 21 patients were included, 10 underwent abdominal MRI before and 3 months after LSG, 11 underwent abdominal MRI before and 1–2 years after LSG. Liver fat fraction (LFF), pancreas fat fraction(PFF) were measured on proton density fat fraction (PDFF) maps at different time points. Fasting blood samples were collected for measurement of triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), plasma glucose and insulin levels. Homeostasis model assessment (HOMA) was used to evaluate insulin resistance (HOMA-IR). Pearson correlation was used to analyze the correlation between different parameters. ResultsLFF and PFF were significantly decreased at 3 months and 1–2 years after LSG along with weight loss, decreased body mass index (BMI) and waist circumference. Though these parameters showed a decreasing trend from 3 months to 1–2 years, but there was no statistical difference. 81.0% patients had fatty liver and 38.1% patients had fatty pancreas at baseline. However, all patients had no fatty liver at 3 months and no fatty pancreas at 1–2 years after LSG. HDL levels were increased, but LDL, TG and insulin levels were decreased 1–2 years after LSG but not at 3 months. LFF was related to fasting insulin and HOMA-IR at baseline but not after LSG. There was no association of PFF with fasting plasma glucose, fasting insulin or HOMA-IR, but ΔPFF was related to Δinsulin and ΔHOMA-IR at 1–2 years after LSG. ConclusionChanges of liver and pancreas fat content in obesity before and after LSG can be quantified by IDEAL-IQ. Treatment with LSG can reverses fatty liver and fatty pancreas in obese patients. In addition, the lipid profile and insulin sensitivity are also improved after LSG along with the decreased of LFF and PFF.

Pancreas fat content, insulin homeostasis and circulating endothelial microparticles inmale essential hypertensive patients.

Thepancreas fat contenthas been poorly investigated in essential hypertension. The authors aim to relatepancreas and liver fat contentwith parameters measuring insulin resistance, beta-cell function and also withmarkers ofendothelial dysfunction and platelet or endothelial cell destruction. The authors studied a group of 40malehypertensive patients with well-controlled blood pressure, maintaining a stable weight, and having not changed their medication during the last year. Pancreas fat content was correlated with HOMA-IR (r=.616, p<.001), HOMA-S (r=-.439, p<.005), beta cell function parameter (r=.457, p<.005), and QUICKI (r=.412, p<.01), whereas liver fat was not patients in thehighest quartileof pancreas fat content had more circulating endothelial microparticles than patients in the other quartiles (median 129 [94.3-200] vs. 60.9 [49.4-88.8], p=.002).However, patients in the highest quartile of the pancreas fat content distribution did not differ from the lowest in hyperemic response after ischemia nor circulating platelet microparticles count. Liver fat content was not related to any of the parameters studied. In a multivariate stepwise binary logistic regression analysis (Wald Method) circulating endothelial microparticles remain significantly associated with pancreas fat content after adjusting for confounding factors, such as tobacco, diabetes mellitus, hypercholesterolemia, or metabolic syndrome. Our results reflect that in essential hypertension,pancreas fat contentis superior toliver fatto study beta-cell functionality and insulin resistance. Moreover, the authors described for the first time thatpancreas fat content isrelated to endothelial cell destruction. Further studies are needed to confirm this point.

Liver fat is superior to visceral and pancreatic fat as a risk biomarker of impaired glucose regulation in overweight/obese subjects.

To investigate the distribution of abdominal fat, particularly ectopic fat accumulation, in relation to glucose metabolism in overweight/obese patients. This study included 257 overweight/obese subjects with body mass index ≥23 kg/m2 . All the subjects underwent an oral glucose tolerance test. Magnetic resonance imaging-proton density fat fraction was used to measure fat accumulation in the liver, pancreas and abdomen. Impaired glucose regulation (IGR) was defined as the presence of prediabetes or diabetes. Liver fat content (LFC) and visceral adipose tissue (VAT) were higher in overweight/obese subjects with diabetes than in those with normal glucose tolerance (NGT). No significant differences were observed in the pancreas fat content and subcutaneous fat area between subjects with NGT and IGR. LFC was an independent risk factor of IGR (odds ratio=1.824 per standard deviation unit, 95% CI 1.242-2.679, p=.002). Compared with the lowest tertile of LFC, the multivariate-adjusted odds ratio for the prevalence of IGR in the highest tertile was 2.842 (95% CI 1.205-6.704). However, no association was observed between the VAT per standard deviation increment and tertiles after adjusting for multiple factors. For discordant visceral and liver fat phenotypes, the high LFC-low VAT and high LFC-high VAT groups had a higher prevalence of IGR than the low LFC-low VAT group. However, there was no difference in the prevalence of IGR between the low LFC-low VAT and low LFC-high VAT groups. Compared with visceral and pancreatic fat content, LFC is a superior risk biomarker for IGR in overweight/obese subjects.

Fatty Pancreas and Cardiometabolic Risk: Response of Ectopic Fat to Lifestyle and Surgical Interventions.

Ectopic fat accumulation in non-adipose organs, such as the pancreas and liver, is associated with an increased risk of cardiometabolic disease. While clinical trials have focused on interventions to decrease body weight and liver fat, ameliorating pancreatic fat can be crucial but successful intervention strategies are not yet defined. We identified twenty-two published studies which quantified pancreatic fat during dietary, physical activity, and/or bariatric surgery interventions targeted at body weight and adipose mass loss alongside their subsequent effect on metabolic outcomes. Thirteen studies reported a significant decrease in body weight, utilising weight-loss diets (n = 2), very low-energy diets (VLED) (n = 2), isocaloric diets (n = 1), a combination of diet and physical activity (n = 2), and bariatric surgery (n = 5) including a comparison with VLED (n = 1). Surgical intervention achieved the largest decrease in pancreatic fat (range: -18.2% to -67.2%) vs. a combination of weight-loss diets, isocaloric diets, and/or VLED (range: -10.2% to -42.3%) vs. diet and physical activity combined (range: -0.6% to -3.9%), with a concurrent decrease in metabolic outcomes. While surgical intervention purportedly is the most effective strategy to decrease pancreas fat content and improve cardiometabolic health, the procedure is invasive and may not be accessible to most individuals. Given that dietary intervention is the cornerstone for the prevention of adverse metabolic health, the alternative approaches appear to be the use of weight-loss diets or VLED meal replacements, which are shown to decrease pancreatic fat and associated cardiometabolic risk.

1184-P: Return to Normal Glucose Control by Weight Loss in Nonobese People with Type 2 Diabetes: The ReTUNE Study

Type 2 diabetes (T2D) in the non-obese has been regarded as etiologically distinct from that in obese people. However, clinical observation suggests that loss of fat mass above a personal fat threshold brings about remission in the same way. ReTUNE aimed to determine what proportion of T2D people with BMI &amp;lt;27kg/m2 could achieve remission, and to assess the fat threshold for this. 25 participants have been studied to date (T2D: 4M/10F, 58.3±2.1years, BMI 24.5±0.6kg/m2; matched nondiabetic controls: n=11). Other types of diabetes were excluded by anti-islet cell antibodies and MODY gene tests (2/14). From baseline, weight loss of 5% was achieved in 2-4 weeks using low calorie diet (800 kcal/day), then 6 weeks of weight maintenance. The cycle of weight loss plus maintenance was repeated 2-3 times until the clinical end point of remission was reached (HbA1c &amp;lt; 6.5%). Only 2 cycles (~10% weight loss) were required in 8/12 participants. The planned decrease in weight (baseline to clinical endpoint: 69.0±3.5 to 60.8±2.9kg, p&amp;lt;0.001) decreased total body fat from 33.1±1.9 to 27.4±2.0% (p&amp;lt;0.001). Fasting plasma glucose decreased from 7.3±0.3 to 6.3±0.3 mmol/l, p&amp;lt;0.05). HbA1c decreased from 7.1±0.2 to 6.5±0.1%, p&amp;lt;0.05 with 8/12 in remission (&amp;lt;6.5%). Fasting plasma insulin decreased (52.2±9.5 to 23.7±3.6 pmol/L, p=0.007) as did plasma triglyceride (1.6±0.2 to 1.0±0.1mmol/L, p=0.002). Liver fat fell from 4.4±0.8 to 1.4±0.1% (p=0.004) becoming similar to 11 matched healthy controls (1.9%). Pancreas fat content in T2D fell (5.1± 0.6 to 4.5±0.6%, p=0.026) towards control levels (3.3±0.3%, p=0.029 vs. T2D at baseline). Post meal insulin sensitivity (Si) and insulin secretion (disposition index and β-cell responsivity Φtot) improved after weight loss. In conclusion, 2/14 people with BMI &amp;lt;27kg/m2 were found to have other diagnoses, and weight loss brought about remission in 8/12 people accompanied by pathophysiological changes similar to those seen during remission in obesity-associated T2D. Disclosure A. Al-mrabeh: None. A. C. Barnes: None. K. M. Irvine: None. T. L. Kelly: Employee; Self; Diabetes Digital Media. K. G. Hollingsworth: None. D. Romeres: None. C. Cobelli: None. R. Taylor: Speaker's Bureau; Self; Novartis AG. Funding Diabetes UK (17/0005645)

1781-P: Remission of Type 2 Diabetes over 2 Years Normalizes Morphology of the Whole Pancreas

In type 2 diabetes, the pancreas is 30% smaller with irregular borders. The lack of rapid postprandial rise in insulin may explain the loss of exocrine tissues mass was postulated to be reversible on remission of diabetes. 90 people (38/52 F/M, 52.8±7.9 years, initial weight 100.2±16.3kg, and BMI 34.7±4.3 kg/m2) were randomized (Diabetes Remission Clinical Trial) to low calorie diet or to continue with routine diabetes management. A group of nondiabetic controls (n=25) matched to the post-diet weight was studied in one occasion. MR techniques were used for anatomical and fat fraction images of the pancreas (3T Philips, Netherlands). Specifically developed methods were used to quantify intrapancreatic fat, change in pancreas volume and irregularity of the border. At baseline, pancreas volume was lower in diabetes (63.8±1.8 vs. 79.8±2.9cm3, p&amp;lt;0.0001). It was unchanged after 5 months, increased at 12 months, and at 24 months had increased further by 12.6±1.5cm3 in responders compared with 4.5±1.3cm3 in non-responders (p&amp;lt;0.0001). Over 24 months, pancreas fat content decreased only in responders (p&amp;lt;0.0001) and responders lost 1.56±0.3% vs. 0.51±0.4% (p&amp;lt;0.05). At 12 months, there were negative correlations between decrease in pancreas fat and increase of insulin secretion (r=-0.55, p&amp;lt;0.0001), and increase in pancreas volume and the decrease of pancreas fat within the whole study (r=-0.35, p=0.02). Reflecting irregularity, Fractal Dimension (FD) of the pancreas borders was higher in the diabetic group (1.116±0.013 vs. 1.097±0.005, p&amp;lt;0.0001) and decreased to 24 months only in those who achieved remission (1.097±0.008, p=0.0003). The low pancreas volume of type 2 diabetes is likely to be related to deficiency of acute insulin secretion over many years of disease progression. Fat removal from the pancreas can restore β cells function and may lead to restoration of exocrine tissues mass via trophic effects of insulin. Pancreas morphology appears to reflect the pathophysiology of type 2 diabetes. Disclosure R. Taylor: Speaker’s Bureau; Self; Novo Nordisk Foundation. S.V. Zhyzhneuskaya: None. C. Peters: Speaker’s Bureau; Self; Sanofi-Aventis. A.C. Barnes: None. K.G. Hollingsworth: None. N. Sattar: Advisory Panel; Self; Amgen, AstraZeneca, Boehringer Ingelheim International GmbH, Eli Lilly and Company, Novo Nordisk A/S, Pfizer Inc., Sanofi. Research Support; Self; Boehringer Ingelheim Pharmaceuticals, Inc. M.E. Lean: None. A. Al-Mrabeh: None. Funding Diabetes UK

Remission of Human Type 2 Diabetes Requires Decrease in Liver and Pancreas Fat Content but Is Dependent upon Capacity for β Cell Recovery

The Diabetes Remission Clinical Trial reported return and persistence of non-diabetic blood glucose control in 46% of people with type 2 diabetes of up to 6 years duration. Detailed metabolic studies were performed on a subgroup (intervention, n= 64; control, n= 26). In the intervention group, liver fat content decreased (16.0%± 1.3% to 3.1%± 0.5%, p< 0.0001) immediately after weight loss. Similarly, plasma triglyceride and pancreas fat content decreased whether or not glucose control normalized. Recovery of first-phase insulin response (0.04[-0.05-0.32] to 0.11[0.0005-0.51] nmol/min/m2, p< 0.0001) defined those who returned to non-diabetic glucose control and this was durable at 12months (0.11[0.005-0.81] nmol/min/m2, p= 0.0001). Responders were similar to non-responders at baseline but had shorter diabetes duration (2.7± 0.3 versus 3.8± 0.4 years; p= 0.02). This study demonstrates that β cell ability to recover long-term function persists after diagnosis, changing the previous paradigm of irreversible loss of β cell function in type 2 diabetes.

Sonographic pancreas echogenicity in cystic fibrosis compared to exocrine pancreatic function and pancreas fat content at Dixon-MRI.

ObjectiveFatty infiltration of the pancreas is a dominating feature in cystic fibrosis (CF). We evaluate the association between pancreatic fat content assessed by Dixon magnetic resonance imaging (MRI), pancreatic echogenicity at ultrasonography (US) and exocrine function in CF patients and healthy controls (HC).Material and methodsTransabdominal US, pancreatic Dixon-MRI and diffusion-weighted imaging (DWI) were performed in 21 CF patients and 15 HCs. Exocrine function was assessed by endoscopic secretin test and fecal elastase.ResultsCF patients were grouped according to exocrine pancreatic function as subjects with normal (CFS: n = 11) or reduced (CFI: n = 10) function. Among CFI 90% (9/10) had visual hyperechogenicity. CFI also had increased echo-level values (p<0.05 vs others). All CFI (10/10) had markedly increased pancreatic fat content estimated by MRI compared to sufficient groups, p<0.001). Among CFS patients and HC, 27% (3/11) and 33% (5/15), respectively, had hyperechoic pancreas. However, all these had low pancreatic fat-content at MRI compared to CFI. In CFI, pancreatic fat content was correlated to ADC (r = -0.93, p<0.001).ConclusionPancreas insufficient CF patients exhibit severe pancreatic fatty-infiltration at MRI and hyperechoic pancreas at US. Pancreas hyperechogenicity in pancreatic sufficient subjects does not co-exist with fatty infiltration at MRI. MRI evaluates pancreatic fatty infiltration more accurately than US and fat infiltration estimated by MRI outperforms sonographic hyper-echogenicity as a marker for exocrine pancreatic failure in CF.

MRI-determined fat content of human liver, pancreas and kidney

To assess and correlate the lipid content of various organs in obese subjects and in persons with a normal body weight. Magnetic resonance spectroscopy and a previously validated gradient echo magnetic resonance imaging method with Dixon's two point technique were used in this study to quantify fat in liver, pancreas as well as kidney. In 36 volunteers with body mass index (BMI) ranging from 20.0 to 42.9 kg/m(2), the median fat content of liver, pancreas and kidney was 2.3% (interquartile range: 0.2%-7.8%), 2.7% (1.0%-6.5%) and 0.7% (0.1%-1.4%), respectively. BMI and subcutaneous fat correlated significantly with liver and pancreas fat content. We show for the first time the significant correlation of liver and pancreas fat content in healthy controls (r = 0.43, P < 0.01). These observations are related to body weight as measured by BMI and the amount of subcutaneous fat. Kidney fat content is very low and correlates with none of the other fat depots. Renal lipid accumulation, unlike the coupled accumulations of fat in liver and pancreas, is not observed in obese subjects. Unlike suggestions made in previous studies, renal lipid accumulation appears not to be involved in the pathogenesis of renal disease in humans.

Quantification of Pancreatic Lipomatosis and Liver Steatosis by MRI: Comparison of In/Opposed-Phase and Spectral-Spatial Excitation Techniques

The goal of the present study was the assessment of pancreatic and hepatic fat content applying 2 established magnetic resonance (MR) imaging techniques: in-phase/opposed-phase gradient-echo MR imaging and fat-selective spectral-spatial gradient-echo imaging. Results of both approaches were compared, and influences of T1- and T2*-related corrections were assessed. The possibility of a correlation between pancreatic lipomatosis and liver steatosis was investigated. Seventeen volunteers at risk for type 2 diabetes (6 male, 11 female; age, 26-70 years; body mass index, 19.4-41.3 kg/m2; mean, 31.7 kg/m2) were examined. Liver and pancreas fat content were quantified with 2 different gradient-echo techniques: one uses a spectral-spatial excitation technique with 6 binomial radio frequency pulses, which combines chemical shift selectivity with simultaneous slice-selective excitation. The other technique based on double-echo chemical shift gradient-echo MR provides in- and opposed-phase images simultaneously. Influences of T1 and individual T2* effects on results using in-phase/opposed-phase imaging were estimated and corrected for, based on additional T2* measurements. The fat content calculated from images recorded with the fat-selective spectral-spatial gradient-echo sequence correlated well with the fat fraction determined with in-phase/opposed-phase imaging and following correction for T1/T2* effects: pancreas r = 0.93 (P < 0.0001) and liver r = 0.96 (P < 0.0001). In-phase/opposed-phase imaging revealed a pancreatic fat content between 1.6% and 22.2% (mean, 8.8% +/- 5.7%) and a hepatic fat fraction between 0.6% and 33.3% (mean, 7.9% +/- 9.1%). The fat-selective spectral-spatial gradient-echo sequence revealed a pancreatic lipid content between 3.4% and 16.1% (mean, 9.8% +/- 4.0%) and a hepatic fat content between 0% and 28.5% (mean, 8.8% +/- 8.3%). With neither technique was a substantial correlation between pancreatic and hepatic fat content found. The presented results suggest that both methods are reliable tools for pancreatic and hepatic fat quantification. However, for reliable assessment of quantitative fat by the in-phase/opposed-phase technique, an additional measurement of T2* seems crucial.