1957-P: The Role of Glucose-Dependent Insulinotropic Polypeptide in Regulation of Splanchnic Blood Flow and Lipid Metabolism in Humans

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1957-P
Author(s):  
ALI ASMAR ◽  
JENS J. HOLST ◽  
MEENA ASMAR
Keyword(s):  
Blood Flow ◽  
Lipid Metabolism ◽  
Splanchnic Blood Flow

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Control Group ◽  
Moderate Exercise ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

Role of EDRF in splanchnic blood flow of normal and chronic portal hypertensive rats

1992 ◽  
Vol 263 (2) ◽  
pp. G149-G154 ◽  
Author(s):  
F. Iwata ◽  
T. Joh ◽  
T. Kawai ◽  
M. Itoh
Keyword(s):  
Blood Flow ◽  
Splanchnic Blood Flow ◽  
Constant Infusion ◽  
Relaxing Factor ◽  
Radioactive Microsphere ◽  
Blood Flow Reduction ◽  
Microsphere Method ◽  
Radioactive Microsphere Method ◽  
Endothelium Derived Relaxing Factor

The role of endogenous endothelium-derived relaxing factor (EDRF) in splanchnic blood flow was assessed in normal and portal vein-stenosed rats (PSRs). Specific and maximal inhibition of EDRF was achieved by intravenous administration of NG-nitro-L-arginine (L-NOARG) as a 1.75 mumol/kg bolus, followed by constant infusion of 1.75 mumol/kg for 20 min. Pretreatment with L-arginine (175 mumol/kg iv) completely blocked both hypertension and the reduction in blood flow induced by L-NOARG. Pretreatment with D-arginine (175 mumol/kg iv) and prazosin (500 micrograms/kg iv) did not attenuate the pressor effect of L-NOARG. These results indicate that L-NOARG selectively blocks EDRF. The blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats was 81.1 +/- 8.7, 199.1 +/- 21.9, 153.3 +/- 20.0, 68.6 +/- 10.6, 79.4 +/- 11.8, and 59.3 +/- 7.8 ml.min-1.100 g-1, respectively, and in PSRs was 141.4 +/- 10.8, 244.0 +/- 10.4, 208.3 +/- 9.8, 126.8 +/- 13.0, 166.9 +/- 16.5, and 94.8 +/- 4.7 ml.min-1.100 g-1, respectively. Blood flow was measured using the radioactive microsphere method. L-NOARG significantly reduced blood flow to the stomach, duodenum, jejunum, ileum, cecum, and colon in control rats by 47, 44, 48, 55, 40, and 41%, respectively, and in PSRs by 30, 27, 36, 33, 28, and 23%, respectively. The magnitude of blood flow reduction in PSRs was lower than in normal rats. These results indicate that EDRF plays an important role in control of the splanchnic circulation, but its effect on the hyperdynamic circulation observed in PSRs is insignificant.

Role of ethanol metabolism in the ethanol-induced increase in splanchnic circulation

1986 ◽  
Vol 250 (4) ◽  
pp. G518-G523 ◽  
Author(s):  
J. P. McKaigney ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
Y. Israel ◽  
H. Orrego
Keyword(s):  
Blood Flow ◽  
Liver Blood Flow ◽  
Portal Blood Flow ◽  
Splanchnic Blood Flow ◽  
Ethanol Metabolism ◽  
Radioactive Microsphere ◽  
Splanchnic Hemodynamics ◽  
Radioactive Microsphere Technique ◽  
Blood Flow Increase

In this study we report the effect on splanchnic hemodynamics of acute oral ethanol at doses ranging from 0.25 to 4.0 g/kg body wt. Flows were determined by use of a radioactive microsphere technique. Ethanol was found to increase portal blood flow by 23-57%. In awake rats this increase reached a plateau at the 0.5 g/kg dose. In ketamine-anesthetized rats, the increase was observed only at doses of 3.0 g/kg or more, with the response at doses of 0.5, 1.0, and 2.0 g/kg being suppressed by ketamine. Inhibition of alcohol dehydrogenase by intra-arterial administration of 4-methylpyrazole resulted in suppression of the liver blood flow increase after ethanol was administered to awake animals. Ethanol in the range of doses studied did not result in changes in blood glucagon levels. Rats fed ethanol-containing diets for 4 wk and withdrawn for 18 h had the same response to acute oral ethanol as did naive rats. It is suggested that ethanol metabolism mediates the effects of ethanol on splanchnic blood flow. An increase in splanchnic blood flow when concurrent with an increase in liver O2 consumption induced by ethanol might protect the liver from hypoxic damage.

scholarly journals Friend or Foe? Spontaneous Portosystemic Shunts in Cirrhosis—Current Understanding and Future Prospects

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Sasidharan Rajesh ◽  
Cyriac Abby Philips ◽  
Rizwan Ahamed ◽  
Jinsha K Abduljaleel ◽  
Dinu Chandran Nair ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Pressure ◽  
Current Understanding ◽  
Splanchnic Blood Flow ◽  
Imaging Biomarker ◽  
Compensatory Mechanism ◽  
Portosystemic Shunts ◽  
High Prevalence ◽  
History Of

Portal hypertension (PHT) in cirrhosis results from increased resistance to splanchnic blood flow secondary to parenchymal and vascular changes within the liver. In an attempt to counteract the increased portal pressure, two mechanisms simultaneously occur: splanchnic vasodilatation and formation of spontaneous portosystemic shunts (SPSS). Long considered to be a compensatory mechanism to decompress the portal venous system, it is now well established that SPSS are not only inefficient in decreasing the portal pressure but also contribute to reduced hepatocyte perfusion and increased splanchnic blood flow and resistance, associated with worsening PHT. Recent studies have described a high prevalence of SPSS in cirrhosis patients, increasing with liver dysfunction, and observed an association between the presence of SPSS and worse clinical outcomes. In cirrhosis patients with preserved liver functions, the presence of SPSS independently increases the risk of hepatic encephalopathy, variceal bleeding, and ascites, and reduces transplant-free survival. Moreover, the presence of SPSS in patients undergoing transjugular intrahepatic portosystemic shunting and liver transplant has been shown to variably affect the postprocedural outcome. This article provides an overview of the current understanding of the role of SPSS in the natural history of liver cirrhosis and their status as a therapeutic target and an imaging biomarker to identify patients at higher risk of developing complications of PHT.

Glucose disposal and lipid metabolism in man: role of thyroid hormones

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S130-S131
Author(s):  
M. J. MÜLLER ◽  
A. G. BURGER ◽  
E. JEQUIER ◽  
K.J. ACHESON
Keyword(s):  
Lipid Metabolism ◽  
Thyroid Hormones ◽  
Glucose Disposal

Genetic background of cholesterol absorption efficacy. The role of Niemann–Pick C1-like 1 receptor and its genetic variation in lipid metabolism

2010 ◽  
Vol 151 (34) ◽  
pp. 1376-1383 ◽  
Author(s):  
Mariann Harangi ◽  
István Balogh ◽  
János Harangi ◽  
György Paragh
Keyword(s):  
Genetic Variation ◽  
Lipid Metabolism ◽  
Genetic Background ◽  
Cholesterol Absorption ◽  
Niemann Pick

A Niemann–Pick C1-like-1 egy szterolfelismerő domént tartalmazó membránfehérje, amelyet nagy számban expresszálnak csúcsi felszínükön a bélhámsejtek. Az utóbbi évek vizsgálatai azt igazolták, hogy ez a fehérje szükséges a szabad koleszterin bejutásához a bélhámsejtekbe a bél lumenéből. Biokémiai vizsgálatok azt igazolták, hogy a Niemann–Pick C1-like-1-hez kötődik az ezetimib, amely egy hatékony koleszterinfelszívódást gátló szer. A bélből történő koleszterinfelszívódás ütemében és az ezetimibkezelés hatékonyságában tapasztalt egyéni eltérések hátterében felmerült néhány Niemann–Pick C1-like-1 génvariáció oki szerepe.

Role of blood flow and impaired autoregulation in the pathogenesis of diabetic retinopathy

Diabetes ◽  
1995 ◽  
Vol 44 (6) ◽  
pp. 603-607 ◽  
Author(s):  
E. M. Kohner ◽  
V. Patel ◽  
S. M. Rassam
Keyword(s):  
Blood Flow ◽  
Diabetic Retinopathy
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