Hemodynamics and metabolism of the in vivo vascularly isolated canine pancreas.

1979 ◽  
Vol 236 (6) ◽  
pp. E626
Author(s):  
R J Alteveer ◽  
M J Jaffe ◽  
J Van Dam
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Venous Blood ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Anesthetized Dogs ◽  
Metabolic Variables ◽  
The Stability ◽  
First Time

Surgical procedures are detailed that have yielded for the first time an in vivo vascularly isolated, autoperfused preparation of the entire pancreas in anesthetized dogs. Previous studies had isolated only part of the pancreas or had resorted to blood-flow techniques not requiring pooled pancreatic venous blood, necessary for metabolic studies of the organ. Pancreatic blood flow (48 ml/min), O2 uptake (180 mumol/min), glucose uptake (51.0 mumol/min), lactate output (6.6 mumol/min), net free fatty acid uptake (2.23 mumol/min), all per 100 g tissue, and various other measured and calculated hemodynamic and metabolic variables were determined on the preparation during control conditions. The stability of the preparation was verified by serial determinations of these parameters and of blood alpha-amylase and beta-glucuronidase levels from 1 to 2.5 h postsurgery. Metabolic rate and glucose uptake were both found to be much higher than in intestinal tissues and approached values characteristic of liver tissue.

Adenosine regulates blood flow and glucose uptake in adipose tissue of dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1127-H1135
Author(s):  
S. E. Martin ◽  
E. L. Bockman
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Indirect Effect ◽  
Glycerol Release ◽  
Anesthetized Dogs ◽  
Tissue Contents ◽  
Fat Pads

Intravenous norepinephrine increases glycerol release and blood flow in adipose tissue. The vasodilation may be an indirect effect of norepinephrine through the production of adenosine. Adenosine increases glucose uptake and inhibits lipolysis in vitro. To test whether adenosine regulates blood flow and/or metabolism in vivo, adenosine deaminase (ADA) was infused intra-arterially into the inguinal fat pads of anesthetized dogs. In unstimulated tissues, ADA (n = 7) significantly increased vascular resistance and significantly decreased glucose uptake compared with the effects of a control (boiled deaminase, n = 6) infusion. ADA completely blocked the norepinephrine-induced vasodilation (n = 6). No potentiation of basal or catecholamine-stimulated lipolysis was observed with ADA. The presence of ADA in the interstitial space was verified by analysis of lymph effluents. Interstitial levels of ADA were inversely correlated with the tissue contents of adenosine. These data support the hypothesis that adenosine is a regulator of blood flow in basal and stimulated adipose tissue. Adenosine also appears to regulate glucose uptake, but not lipolysis, in vivo.

scholarly journals Role of hypoxia in obesity-induced disorders of glucose and lipid metabolism in adipose tissue

2009 ◽  
Vol 296 (2) ◽  
pp. E333-E342 ◽  
Author(s):  
Jun Yin ◽  
Zhanguo Gao ◽  
Qing He ◽  
Dequan Zhou ◽  
ZengKui Guo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Interstitial Oxygen ◽  
Obese Mice ◽  
Cell Type Specificity

Recent studies suggest that adipose tissue hypoxia (ATH) may contribute to endocrine dysfunction in adipose tissue of obese mice. In this study, we examined hypoxia's effects on metabolism in adipocytes. We determined the dynamic relationship of ATH and adiposity in ob/ob mice. The interstitial oxygen pressure (Po2) was monitored in the epididymal fat pads for ATH. During weight gain from 39.5 to 55.5 g, Po2 declined from 34.8 to 20.1 mmHg, which are 40–60% lower than those in the lean mice. Insulin receptor-β (IRβ) and insulin receptor substrate-1 (IRS-1) were decreased in the adipose tissue of obese mice, and the alteration was observed in 3T3-L1 adipocytes after hypoxia (1% oxygen) treatment. Insulin-induced glucose uptake and Akt Ser473 phosphorylation was blocked by hypoxia in the adipocytes. This effect of hypoxia exhibited cell type specificity, as it was not observed in L6 myotubes and βTC6 cells. In response to hypoxia, free fatty acid (FFA) uptake was reduced and lipolysis was increased in 3T3-L1 adipocytes. The molecular mechanism of decreased fatty acid uptake may be related to inhibition of fatty acid transporters (FATP1 and CD36) and transcription factors (PPARγ and C/EBPα) by hypoxia. The hypoxia-induced lipolysis was observed in vivo after femoral arterial clamp. Necrosis and apoptosis were induced by hypoxia in 3T3-L1 adipocytes. These data suggest that ATH may promote FFA release and inhibit glucose uptake in adipocytes by inhibition of the insulin-signaling pathway and induction of cell death.

scholarly journals Prep1 Deficiency Induces Protection from Diabetes and Increased Insulin Sensitivity through a p160-Mediated Mechanism

2008 ◽  
Vol 28 (18) ◽  
pp. 5634-5645 ◽  
Author(s):  
Francesco Oriente ◽  
Luis Cesar Fernandez Diaz ◽  
Claudia Miele ◽  
Salvatore Iovino ◽  
Silvia Mori ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Normal Glucose Tolerance ◽  
Glucose Disposal ◽  
Protein Levels ◽  
Normal Glucose ◽  
Enhanced Expression ◽  
The Stability

ABSTRACT We have examined glucose homeostasis in mice hypomorphic for the homeotic transcription factor gene Prep1. Prep1-hypomorphic (Prep1 i / i ) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance. In addition, these mice exhibit protection from streptozotocin-induced diabetes and enhanced insulin sensitivity with improved glucose uptake and insulin-dependent glucose disposal by skeletal muscle. This muscle phenotype does not depend on reduced expression of the known Prep1 transcription partner, Pbx1. Instead, in Prep1 i / i muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160. Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1α, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle. Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1. In vivo skeletal muscle delivery of p160 cDNA in Prep1 i / i mice also reverses the molecular phenotype. Finally, we show that Prep1 controls the stability of the p160 protein. We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.

Effects of PACAP1–27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism

2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi
Keyword(s):  
Endocrine Pancreas ◽  
Venous Blood ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Cholinergic Mechanism ◽  
Insulin And Glucagon Secretion ◽  
Anesthetized Dogs

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.

scholarly journals Testicular microvascular flow is altered in Klinefelter syndrome and predicts circulating testosterone

2021 ◽  
Author(s):  
Francesco Carlomagno ◽  
Carlotta Pozza ◽  
Marta Tenuta ◽  
Riccardo Pofi ◽  
Luigi Tarani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Klinefelter Syndrome ◽  
Mean Transit Time ◽  
Venous Blood ◽  
Experimental Studies ◽  
Principal Component ◽  
Endocrine Function ◽  
Venous Blood Flow ◽  
Testicular Blood Flow

ABSTRACTContextExperimental studies on Klinefelter syndrome (KS) reported increased intratesticular testosterone (T) levels coexisting with reduced circulating levels. Abnormalities in testicular microcirculation have been claimed; however, no studies investigated in vivo testicular blood flow dynamics in humans with KS.ObjectiveTo analyze the testicular microcirculation in KS by contrast-enhanced ultrasonography (CEUS) and correlate vascular parameters with endocrine function.Design and SettingProspective study. University Settings.Patients51 testicular scans, 17 testes from 10 T-naïve subjects with KS and 34 testes from age-matched eugonadal men (CNT) who underwent CEUS for incidental nonpalpable testicular lesions.Main OutcomesCEUS kinetic parameters.ResultsCEUS revealed slower testicular perfusion kinetics in subjects with KS than in age-matched CNT. Specifically, the wash-in time (Tin, p = 0.008), mean transit time (MTT, p = 0.008), time to peak (TTP, p < 0.001), and washout time (Tout 50%, p = 0.008) were all prolonged. Faster testicular blood flow was associated with higher total T levels. Principal component analysis and multiple linear regression analyses confirmed the findings, and supported a role for reduced venous blood flow as independent predictor of total T levels.ConclusionsTesticular venous blood flow is altered in KS and independently predicts T peripheral release.

Adenosine potentiates insulin-stimulated myocardial glucose uptake in vivo

1988 ◽  
Vol 254 (5) ◽  
pp. H970-H975 ◽  
Author(s):  
W. R. Law ◽  
R. M. Raymond
Keyword(s):  
Blood Flow ◽  
Glucose Uptake ◽  
Coronary Blood Flow ◽  
Metabolic Regulation ◽  
Metabolic Response ◽  
Dose Response Relationship ◽  
Circumflex Artery ◽  
Myocardial Glucose Uptake

Myocardial adenosine (ADO) has long been regarded as a regulator of coronary blood flow. In other tissues, such as adipose and skeletal muscle, much attention has focused on the role of ADO as a metabolic regulator of the actions of insulin. In the present study, we determined the effect of ADO infusion on insulin-stimulated myocardial glucose uptake (MGU). Mongrel dogs of either sex were instrumented to obtain arterial-coronary sinus differences for glucose, lactate, and oxygen. These were multiplied by circumflex artery blood flow (Q) to obtain uptake values. Measurements were made before and during hyperinsulinemic (4 U/min)-euglycemic clamp (clamp) with intracoronary infusions of saline, ADO, adenosine deaminase (ADA), or nitroprusside (NP). During clamp, MGU increased from a basal value of 3.0 +/- 0.8 mg/min (mean +/- SE) to 5.53 +/- 0.8 mg/min. Adenosine infusion potentiated this response, raising MGU further to 9.02 +/- 1.1 mg/min while not significantly affecting lactate or oxygen uptakes. Infusion of ADA confirmed the specificity of the response by blocking the metabolic effect of exogenously infused ADO. When NP was infused, Q increased significantly without altering MGU, indicating that the metabolic response to ADO was independent of the changes it caused in Q. A dose-response relationship existed between ADO and insulin-stimulated MGU. The metabolic response to ADO was more sensitive than the vasodilator response. It is concluded that ADO acts as a regulator of insulin in heart. This metabolic regulation occurs independent of changes in coronary blood flow.

scholarly journals Protein Kinase D1 Is Essential for Contraction-induced Glucose Uptake but Is Not Involved in Fatty Acid Uptake into Cardiomyocytes

2011 ◽  
Vol 287 (8) ◽  
pp. 5871-5881 ◽  
Author(s):  
Ellen Dirkx ◽  
Robert W. Schwenk ◽  
Will A. Coumans ◽  
Nicole Hoebers ◽  
Yeliz Angin ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Kinase ◽  
Glucose Uptake ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Protein Kinase D1

Increased glucose uptake by intestinal mucosa and muscularis in hypermetabolic sepsis

1991 ◽  
Vol 261 (2) ◽  
pp. G287-G294 ◽  
Author(s):  
C. H. Lang ◽  
J. C. Obih ◽  
G. J. Bagby ◽  
J. N. Bagwell ◽  
J. J. Spitzer
Keyword(s):  
Blood Flow ◽  
Gastrointestinal Tract ◽  
Glucose Uptake ◽  
Intestinal Blood Flow ◽  
Similar Extent ◽  
Relative Contribution ◽  
Entire Small Intestine ◽  
Elevated Rate ◽  
Small And Large Intestine

The purpose of the present study was to determine the following: 1) whether the sepsis-induced increase in glucose uptake was a generalized response along the entire length of the gastrointestinal tract; 2) the relative contribution of the mucosa and muscularis to the enhanced uptake; and 3) whether reducing intestinal blood flow would attenuate the elevated rate of glucose uptake. Hypermetabolic sepsis increased in vivo glucose uptake in all sections of the gastrointestinal tract (57-93%) except the stomach. The rates of glucose uptake per gram of tissue by the mucosa and muscularis were not different. However, because the mucosa accounted for the majority of the whole intestine mass, this layer was responsible for 76-78% of the glucose uptake by the entire small intestine. Intestinal blood flow, determined with the use of radiolabeled microspheres, increased by 127% in sepsis. In both groups, approximately 70% of the total intestinal blood flow was distributed to the mucosa. Somatostatin was infused to produce splanchnic vasoconstriction and decreased the sepsis-induced increment in intestinal flow to the mucosa and muscularis (38 and 54%), whereas the enhanced rate of glucose uptake was not altered. Somatostatin also produced a severe insulinopenia. These results indicate that hypermetabolic sepsis increases glucose uptake to a similar extent along the length of the small and large intestine and that the majority of this increase is due to an enhanced uptake by the mucosa.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of exercise training on in vivo insulin-stimulated glucose uptake in intra-abdominal adipose tissue in rats

2000 ◽  
Vol 278 (1) ◽  
pp. E25-E34 ◽  
Author(s):  
L. H. Enevoldsen ◽  
B. Stallknecht ◽  
J. D. Fluckey ◽  
H. Galbo
Keyword(s):  
Insulin Resistance ◽  
Blood Flow ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Insulin Resistance Syndrome ◽  
Fat Depots ◽  
Lower Glucose ◽  
Interstitial Glucose ◽  
And Training

Intra-abdominal obesity may be crucial in the pathogenesis of the insulin-resistance syndrome, and training may alleviate this condition. We compared insulin-mediated glucose uptake in vivo in three intra-abdominal adipose tissues (ATs; retroperitoneal, parametrial, and mesenteric) and in subcutaneous AT and also studied the effect of training. Rats were either swim trained (15 wk, n = 9) or sedentary ( n = 16). While the rats were under anesthesia, a hyperinsulinemic (∼900 pM), euglycemic clamp was carried out and local glucose uptake was measured by both the 2-deoxy-d-[3H]glucose and microdialysis techniques. Blood flow was measured by microspheres. Upon insulin stimulation, blood flow generally decreased in AT. Flow was higher in mesenteric tissue than in other ATs, whereas insulin-mediated glucose uptake did not differ between ATs. Training doubled the glucose infusion rate during hyperinsulinemia, in part, reflecting an effect in muscle. During hyperinsulinemia, interstitial glucose concentrations were lower, glucose uptake per 100 g of tissue was higher in AT in trained compared with sedentary rats, and training influenced glucose uptake identically in all ATs. In conclusion, differences between ATs in insulin sensitivity with respect to glucose uptake do not explain that insulin resistance is associated with intra-abdominal rather than subcutaneous obesity. Furthermore, training may be beneficial by enhancing insulin sensitivity in intra-abdominal fat depots.

Sign in / Sign up

Export Citation Format

Share Document