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.

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.

THE STIMULATING EFFECTS OF ADRENALINE AND ANTERIOR PITUITARY HORMONES ON THE RELEASE OF FREE FATTY ACIDS FROM ADIPOSE TISSUE

1962 ◽  
Vol 25 (2) ◽  
pp. 189-198 ◽  
Author(s):  
R. M. BUCKLE
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Pituitary Hormones ◽  
Thyroid Stimulating Hormone ◽  
Adrenocorticotrophic Hormone ◽  
Fat Pads

SUMMARY The quantity of free fatty acids (FFA) released from rat epididymal fat pads in vitro and their concentration within the tissue were determined. The addition of adrenaline, adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH) and growth hormone (GH) each increased the release of FFA, and their respective minimum effective concentrations were 0·125, 0·004, 0·5 and 1·25 μg./ml. of medium. In every case, the increased release of FFA was associated with a rise in the quantity present within the pads, and the amount released closely paralleled their concentration within the tissue. It is suggested that the stimulatory effect of all four hormones on the release of FFA from adipose tissue is largely a manifestation of their activity of increasing the concentration of FFA within the cells, and this they do by facilitating the net conversion of storage triglyceride to fatty acid. The significance of the relative activities of the hormones in vitro is discussed and compared with their fatty acid mobilizing effects in vivo.

The PPARγ agonist rosiglitazone enhances rat brown adipose tissue lipogenesis from glucose without altering glucose uptake

2009 ◽  
Vol 296 (5) ◽  
pp. R1327-R1335 ◽  
Author(s):  
William T. Festuccia ◽  
Pierre-Gilles Blanchard ◽  
Véronique Turcotte ◽  
Mathieu Laplante ◽  
Meltem Sariahmetoglu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Mrna Levels ◽  
Pparγ Agonist ◽  
Brown Adipose ◽  
Lipin 1 ◽  
The Impact

We investigated the mechanisms whereby peroxisome proliferator-activated receptor-γ (PPARγ) agonism affects glucose and lipid metabolism in brown adipose tissue (BAT) by studying the impact of PPARγ activation on BAT glucose uptake and metabolism, lipogenesis, and mRNA levels plus activities of enzymes involved in triacylglycerol (TAG) synthesis. Interscapular BAT of rats treated or not with rosiglitazone (15 mg·kg−1·day−1, 7 days) was evaluated in vivo for glucose uptake and lipogenesis and in vitro for glucose metabolism, gene expression, and activities of glycerolphosphate acyltransferase (GPAT), phosphatidate phosphatase-1 (PAP or lipin-1), and diacylglycerol acyltransferase (DGAT). Rosiglitazone increased BAT mass without affecting whole tissue glucose uptake. BAT glycogen content (−80%), its synthesis from glucose (−50%), and mRNA levels of UDP-glucose pyrophosphorylase (−40%), which generates UDP-linked glucose for glycogen synthesis, were all reduced by rosiglitazone. In contrast, BAT TAG-glycerol synthesis in vivo and glucose incorporation into TAG-glycerol in vitro were stimulated by the agonist along with the activities and mRNA levels of glycerol 3-phosphate-generating phosphoenolpyruvate carboxykinase and glycerokinase. Furthermore, rosiglitazone markedly increased the activities of GPAT and DGAT but not those of lipin-1-mediated PAP-1, enzymes involved in the sequential acylation of glycerol 3-phosphate and TAG synthesis. Because an adequate supply of fatty acids is essential for BAT nonshivering thermogenesis, the enhanced ability of BAT to synthesize TAG under PPARγ activation may constitute an important mechanism by which lipid substrates are stored in preparation for an eventual thermogenic activation.

THE INFLUENCE OF DEXAMETHASONE ON ADIPOSE TISSUE METABOLISM IN VITRO

1967 ◽  
Vol 39 (3) ◽  
pp. 329-343 ◽  
Author(s):  
R. E. YORKE
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Concentration Ratio ◽  
Maximal Rate ◽  
Small Reduction ◽  
Tissue Content ◽  
Lactate And Pyruvate ◽  
Kinetics Of ◽  
Fat Pads

SUMMARY The influence of dexamethasone on the metabolism of incubated rat epididymal fat pads was investigated. In the presence of dexamethasone the glucose uptake and lactate and pyruvate outputs of the tissue, the concentration ratio lactate: pyruvate in the medium at the end of the incubation and the tissue content of glycogen, glucose-6-phosphate and l-glycerol-3-phosphate were decreased. No changes were observed in the rate of pyruvate utilization, the tissue content of ATP, ADP, AMP and citrate or the output of glycerol. Studies on the kinetics of glucose uptake indicated that in the presence of dexamethasone the maximal rate of uptake (Vmax) was decreased from 0·63 mg./g. wet tissue/hr. to 0·31 mg./g. wet tissue/hr., whereas the glucose concentration in the medium for half-maximal uptake (Ku) (0·29 mg./ml.) was not changed. These results confirmed that the effects of dexamethasone on the tissue were slow in onset, only appearing after 2 hr. pre-incubation with the hormone, but insulin (500 μ-u./ml.) released completely and rapidly the inhibition of glucose uptake induced by dexamethasone. Dexamethasone was also found to cause a small reduction in the incorporation of [1-14C]glycine into adipose tissue protein and nucleic acid fractions.

Effect of pioglitazone on vascular reactivity in vivo and in vitro

1996 ◽  
Vol 270 (3) ◽  
pp. R660-R666 ◽  
Author(s):  
T. A. Kotchen ◽  
H. Y. Zhang ◽  
S. Reddy ◽  
R. G. Hoffmann
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Sprague Dawley ◽  
Vasoactive Agents ◽  
Sprague Dawley Rats ◽  
Pressor Responses

Pioglitazone (a thiazolidinedione derivative) increases insulin sensitivity and prevents hypertension in the Dahl-salt-sensitive (S) rat. The present study was undertaken to determine if pioglitazone modulates pressor responsiveness to vasoactive agents, both in vivo and in vitro. In vivo, pretreatment with pioglitazone inhibited (P < 0.02) pressor responses to both norepinephrine and angiotensin II in conscious Dahl-S, but not in Sprague-Dawley rats. In vitro, pioglitazone augmented the capacity of insulin to inhibit pressor responses of strips of thoracic aortas to norepinephrine, but not to angiotensin. Additionally, in vitro, incubation with insulin plus pioglitazone augmented acetylcholine-induced, but not nitroprusside-induced vasodilation. Pioglitazone pretreatment increased (P < 0.001) in vitro insulin-stimulated glucose uptake in adipose tissue, but not in thoracic aortas of Dahl-S. We hypothesize that pioglitazone attenuates hypertension by modulating the effects of insulin on vascular function, resulting in both blunted vasoconstriction and augmented acetylcholine-induced vasodilation. These alterations are not accounted for by an effect of pioglitazone on glucose uptake by vascular smooth muscle.

scholarly journals Relationship of brown adipose tissue perfusion and function: a study through β2-adrenoreceptor stimulation

2016 ◽  
Vol 120 (8) ◽  
pp. 825-832 ◽  
Author(s):  
Laura Ernande ◽  
Kristin I. Stanford ◽  
Robrecht Thoonen ◽  
Haihua Zhang ◽  
Maëva Clerte ◽  
...  
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Glucose Uptake ◽  
Direct Effect ◽  
Brown Adipocytes ◽  
Bat Activity ◽  
Brown Adipose

Brown adipose tissue (BAT) activation increases glucose and lipid consumption; as such, it is been considered as a potential therapy to decrease obesity. BAT is highly vascularized and its activation is associated with a necessary increase in blood flow. However, whether increasing BAT blood flow per se increases BAT activity is unknown. To examine this hypothesis, we investigated whether an isolated increase in BAT blood flow obtained by β2-adrenoreceptor (β2-AR) stimulation with salbutamol increased BAT activity. BAT blood flow was estimated in vivo in mice using contrast-enhanced ultrasound. The absence of direct effect of salbutamol on the function of isolated brown adipocytes was assessed by measuring oxygen consumption. The effect of salbutamol on BAT activity was investigated by measuring BAT glucose uptake in vivo. BAT blood flow increased by 2.3 ± 0.6-fold during β2-AR stimulation using salbutamol infusion in mice ( P = 0.003). β2-AR gene expression was detectable in BAT but was extremely low in isolated brown adipocytes. Oxygen consumption of isolated brown adipocytes did not change with salbutamol exposure, confirming the absence of a direct effect of β2-AR agonist on brown adipocytes. Finally, β2-AR stimulation by salbutamol increased BAT glucose uptake in vivo (991 ± 358 vs. 135 ± 49 ng glucose/mg tissue/45 min in salbutamol vs. saline injected mice, respectively, P = 0.046). In conclusion, an increase in BAT blood flow without direct stimulation of the brown adipocytes is associated with increased BAT metabolic activity. Increasing BAT blood flow might represent a new therapeutic target in obesity.

Relationships between in vivo and in vitro lipid metabolism in lactating goats

2000 ◽  
Vol 51 (1) ◽  
pp. 139 ◽  
Author(s):  
F. R. Dunshea ◽  
T. E. Trigg ◽  
K. D. Chandler ◽  
A. W. Bell
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Early Lactation ◽  
Glycerol Release ◽  
Dairy Goats ◽  
Entry Rate ◽  
Stage Of Lactation ◽  
Lactating Goats

Multiparous Sannen dairy goats were used to compare in vivo and in vitro lipid metabolism. Goats were infused simultaneously with a mixture of [2-3H]-glycerol and of [1-14C]-palmitic, -stearic, and -oleic acid complexed in plasma in early (Day 11, n = 4), mid (Day 37, n = 4), and late (Day 80, n = 3) lactation to determine in vivo lipid kinetics. Perirenal adipose tissue biopsies were obtained and used to measure in vitro lipid kinetics under both basal and norepinephrine-stimulated conditions. Plasma non-esterified fatty acid (NEFA) concentrations and NEFA entry rate were higher (P < 0.05) during early compared with mid and late lactation. Plasma glucose and glycerol concentrations and glycerol entry rate were not different between stages of lactation. Although variable, in vitro lipogenesis increased more than 10-fold (P = 0.077) between early and late lactation, whereas there were no significant differences between NEFA and glycerol release at any stage of lactation. In vitro lipid metabolism, when expressed per gram of adipose tissue, was poorly correlated with in vivo lipid. However, when in vitro NEFA release was extrapolated to the whole animal the correlations were markedly improved. These data demonstrate that the reduction in lipid reserves which occurs during early lactation is the result of increased NEFA mobilisation and reduced lipogenesis rather than increased lipolysis. Although more variable than in vivo measures of lipid metabolism, in vitro metabolism of adipose tissue can reflect metabolic status.

Insulin binding and action in adipocytes in vitro in relation to insulin action in vivo in young and middle-aged subjects

1986 ◽  
Vol 113 (1) ◽  
pp. 88-92 ◽  
Author(s):  
Hannele Yki-Jarvinen ◽  
Tuula Kiviluoto ◽  
Esko A. Nikkila
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Transport ◽  
Young Group ◽  
Middle Aged ◽  
Young Subjects ◽  
Aged Subjects

Abstract. The effect of age on glucose metabolism in vivo was compared to that found in adipocytes in vitro in young (n = 8, age 23 to 31 years) and middle-aged (n = 7, age 37 to 55 years) non-diabetic subjects. During the OGTT, the incremental glucose or insulin areas did not differ significantly between the groups. Fasting and 2 h plasma glucose (P < 0.01) and the 2 h plasma insulin (P < 0.05) levels were, however, slightly higher in the middle-aged than in the young group. During iv induced hyperinsulinaemia (~ 85 mU/l), rates of glucose uptake were comparable between the middle-aged (6.32 ± 0.94 mg/kg/min) and the young subjects (7.56 ± 0.78 mg/kg/min, P > 0.5). In fat cells, both basal and insulin stimulated rates of glucose transport were 35% lower (P < 0.05) in the middle-aged than in the young subjects. Basal and insulin stimulated rates of glucose oxidation and lipogenesis were both markedly lower (P <0.01) in the middle-aged than in the young group. The rates of glucose transport, oxidation and lipogenesis were inversely related to age, whereas none of these parameters was related to fat cell size. In conclusion, adipocyte glucose metabolism in middle-aged healthy subjects was markedly impaired. In contrast, rates of glucose uptake during iv hyperinsulinaemia and glucose responses during hyperinsulinaemia in the OGTT were comparable in young and middle-aged subjects. These results indicate first, that changes in adipose tissue glucose metabolism by aging do not parallel changes in whole body glucose metabolism and thus are specific for adipose tissue. Secondly, insulin-mediated glucose uptake is not reduced in middle-aged subjects. Thus, the small elevation in fasting and 2-h glucose levels may reflect a reduction in glucose uptake by non-insulin dependent pathways by aging.

ATP-sensitive potassium channels participate in glucose uptake in skeletal muscle and adipose tissue

2002 ◽  
Vol 283 (6) ◽  
pp. E1178-E1184 ◽  
Author(s):  
Takashi Miki ◽  
Kohtaro Minami ◽  
Li Zhang ◽  
Mizuo Morita ◽  
Tohru Gonoi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Skeletal Muscles ◽  
Glucagon Secretion ◽  
Channel Activity ◽  
Wild Type ◽  
Insulin And Glucagon Secretion ◽  
Uptake Experiment

ATP-sensitive potassium (KATP) channels are known to be critical in the control of both insulin and glucagon secretion, the major hormones in the maintenance of glucose homeostasis. The involvement of KATPchannels in glucose uptake in the target tissues of insulin, however, is not known. We show here that Kir6.2(−/−) mice lacking Kir6.2, the pore-forming subunit of these channels, have no KATPchannel activity in their skeletal muscles. A 2-deoxy-[3H]glucose uptake experiment in vivo showed that the basal and insulin-stimulated glucose uptake in skeletal muscles and adipose tissues of Kir6.2(−/−) mice is enhanced compared with that in wild-type (WT) mice. In addition, in vitro measurement of glucose uptake indicates that disruption of the channel increases the basal glucose uptake in Kir6.2(−/−) extensor digitorum longus and the insulin-stimulated glucose uptake in Kir6.2(−/−) soleus muscle. In contrast, glucose uptake in adipose tissue, measured in vitro, was similar in Kir6.2(−/−) and WT mice, suggesting that the increase in glucose uptake in Kir6.2(−/−) adipocytes is mediated by altered extracellular hormonal or neuronal signals altered by disruption of the KATP channels.

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