Pancreatic Metabolism, Blood Flow, and β-Cell Function in Obese Humans

Honka, Henri; Hannukainen, Jarna C.; Tarkia, Miikka; Karlsson, Henry K.; Saunavaara, Virva; Soinio, Minna; Mikkola, Kirsi; Kudomi, Nobu; Oikonen, Vesa; Haaparanta‐Solin, Merja; Roivainen, Anne; Parkkola, Riitta; Iozzo, Patricia; Nuutila, Pirjo

doi:10.1210/jc.2013-4369

Cited by 33 publications

(23 citation statements)

References 34 publications

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“…In order to reduce possible partial volume effect, the ROIs were delineated slightly inside the pancreatic contour. CT VOIs were transferred to co-registered [ 15 Portal and arterial hepatic perfusion were calculated and used as comparators [1]. The data of one healthy individual could not be fitted accurately to this model and was therefore excluded.…”

Section: Methodsmentioning

confidence: 99%

“…Positron emission tomography (PET) with radioactive labelled water ([ 15 O]H 2 O) as a tracer is a well-established tool to study changes in perfusion in human organs and has previously been used to study pancreatic perfusion under basal conditions [1,2]. Pancreatic perfusion is normally closely related to tissue function, for example secretin, a hormone which stimulates exocrine secretion, also increases pancreatic perfusion in humans [3].…”

Section: Introductionmentioning

confidence: 99%

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Pancreatic perfusion and subsequent response to glucose in healthy individuals and patients with type 1 diabetes

et al. 2016

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Aims/hypothesis The aim of this study was to investigate pancreatic perfusion and its response to a glucose load in patients with type 1 diabetes mellitus compared with non-diabetic ('healthy') individuals. Methods Eight individuals with longstanding type 1 diabetes and ten sex-, age-and BMI-matched healthy controls underwent dynamic positron emission tomography scanning with 15 O-labelled water before and after intravenous administration of glucose. Perfusion in the pancreas was measured. Portal and arterial hepatic perfusion were recorded as references. Results Under fasting conditions, total pancreatic perfusion was on average 23% lower in the individuals with diabetes compared with healthy individuals. Glucose increased total pancreatic and portal hepatic blood perfusion in healthy individuals by 48% and 38%, respectively. In individuals with diabetes there was no significant increase in either total pancreatic or portal hepatic perfusion.Conclusions/interpretation Individuals with type 1 diabetes have reduced basal pancreatic perfusion and a severely impaired pancreatic and splanchnic perfusion response to intravenous glucose stimulation.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pancreatic perfusion and subsequent response to glucose in healthy individuals and patients with type 1 diabetes

et al. 2016

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“…Ten studies, 2,9,[11][12][13]15,17,18,20,22 which included a total of 1427 individuals, reported correlation coefficients between markers in blood and percentage of pancreatic fat. Correlation coefficients of 15 markers measured during the fasting state were available for meta-analysis (Table 2).…”

Section: Pooled Correlations Of Biological Markers With Pancreatic Fatmentioning

confidence: 99%

Ectopic fat accumulation in the pancreas and its biomarkers: A systematic review and meta‐analysis

Singh

Yoon

Poppitt

et al. 2017

Diabetes Metabolism Res

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Presence of fat in the pancreas increases the risk of metabolic co-morbidities. Detection and quantification of pancreatic fat is not a routine clinical practice, at least in part because of need to use expensive imaging techniques. We aimed to systematically review common markers of pancreatic fat in blood and to investigate differences in these markers associated with fatty pancreas. The search was conducted in 3 databases (EMBASE, Scopus, and MEDLINE). Studies in humans were eligible for inclusion if they reported on biological markers and percentage of pancreatic fat or fatty pancreas prevalence. Data were pooled for correlation and effect size meta-analysis. A total of 17 studies including 11 967 individuals were eligible for meta-analysis. Markers of lipid metabolism, including circulating triglycerides (r = 0.38 [95% confidence interval (CI) 0.31, 0.46]) and high-density lipoprotein cholesterol (r = -0.33 [95% CI -0.35, -0.31]), and markers of glucose metabolism, including glycated haemoglobin (r = 0.39 [95% CI 0.30, 0.48], insulin (r = 0.38 [95% CI 0.33, 0.43]), and homeostasis model assessment-insulin resistance (r = 0.37 [95% CI 0.30, 0.44], yielded the best correlations with percentage of pancreatic fat. Further, effect size analysis showed large and medium effects for the above markers of lipid and glucose metabolism. Circulating levels of triglycerides and glycated haemoglobin appear to be the best currently available markers of pancreatic fat. The approach of non-invasive and accurate detection of pancreatic fat by blood analysis should be further explored in the future, by investigating other potential biological markers of pancreatic fat.

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“…Honka et al have recently studied pancreatic metabolism and blood flow in obese subjects, using positron emission tomography (PET) [128]. The obese individuals showed increased pancreatic fatty acid uptake and fat accu Legend: CT -computed tomography, DM -diabetes mellitus, FP -fatty pancreas, IFG -impaired fasting glucose, IGT -impaired glucose tolerance, MRI -magnetic resonance imaging, MRS -magnetic resonance spectroscopy, NDM -non-diabetes mellitus, NGT -normal glucose tolerance, HOMA-IR -homeostasis model assessment of insulin resistance, HOMA-β -homeostatis model assessment of beta-cell function, PET -positron emission tomography, T2D -type 2 diabetes.…”

Section: Pancreatic Fat Beta-cell Function and Glucose Intolerancementioning

confidence: 99%

“…Honka et al have recently studied pancreatic metabolism and blood flow in obese subjects, using positron emission tomography (PET) [128]. The obese individuals showed increased pancreatic fatty acid uptake and fat accumulation and reduced pancreatic blood flow; both of these effects were inversely associated with beta-cell function [128].…”

Section: Pancreatic Fat Beta-cell Function and Glucose Intolerancementioning

confidence: 99%

Pancreas Volume and Fat Deposition in Diabetes and Normal Physiology: Consideration of the Interplay Between Endocrine and Exocrine Pancreas

Saisho¹

2016

Rev Diabet Stud

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■ AbstractThe pancreas is comprised of exocrine and endocrine components. Despite the fact that they are derived from a common origin in utero, these two compartments are often studied individually because of the different roles and functions of the exocrine and endocrine pancreas. Recent studies have shown that not only type 1 diabetes (T1D), but also type 2 diabetes (T2D), is characterized by a deficit in beta-cell mass, suggesting that pathological changes in the pancreas are critical events in the natural history of diabetes. In both patients with T1D and those with T2D, pancreas mass and exocrine function have been reported to be reduced. On the other hand, pancreas volume and pancreatic fat increase with obesity. Increased beta-cell mass with increasing obesity has also been observed in humans, and ectopic fat deposits in the pancreas have been reported to cause beta-cell dysfunction. Moreover, neogenesis and transdifferentiation from the exocrine to the endocrine compartment in the postnatal period are regarded as a source of newly formed beta-cells. These findings suggest that there is important interplay between the endocrine and exocrine pancreas throughout life. This review summarizes the current knowledge on physiological and pathological changes in the exocrine and endocrine pancreas (i.e., beta-cell mass), and discusses the potential mechanisms of the interplay between the two compartments in humans to understand the pathophysiology of diabetes better.

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Pancreatic Metabolism, Blood Flow, and β-Cell Function in Obese Humans

Abstract: Obesity leads to changes in pancreatic energy metabolism with a substrate shift from glucose to FAs. In morbidly obese humans, impaired pancreatic blood flow may contribute to β-cell dysfunction and in the pathogenesis of type 2 diabetes.

Cited by 33 publications

References 34 publications

Pancreatic perfusion and subsequent response to glucose in healthy individuals and patients with type 1 diabetes

Pancreatic perfusion and subsequent response to glucose in healthy individuals and patients with type 1 diabetes

Ectopic fat accumulation in the pancreas and its biomarkers: A systematic review and meta‐analysis

Pancreas Volume and Fat Deposition in Diabetes and Normal Physiology: Consideration of the Interplay Between Endocrine and Exocrine Pancreas

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