scholarly journals Acute Hypercortisolemia Exerts Depot-Specific Effects on Abdominal and Femoral Adipose Tissue Function

2017 ◽  
Vol 102 (4) ◽  
pp. 1091-1101 ◽  
Author(s):  
Konstantinos N. Manolopoulos ◽  
Michael W. O’Reilly ◽  
Iwona J. Bujalska ◽  
Jeremy W. Tomlinson ◽  
Wiebke Arlt
Keyword(s):  
Adipose Tissue ◽  
Tissue Blood Flow ◽  
Healthy Male ◽  
Double Blind ◽  
Nonesterified Fatty Acids ◽  
Abdominal Adipose Tissue ◽  
Triglyceride Hydrolysis ◽  
Specific Effects ◽  
In Vivo Assessment

Abstract Context: Glucocorticoids have pleiotropic metabolic functions, and acute glucocorticoid excess affects fatty acid metabolism, increasing systemic lipolysis. Whether glucocorticoids exert adipose tissue depot-specific effects remains unclear. Objective: To provide an in vivo assessment of femoral and abdominal adipose tissue responses to acute glucocorticoid administration. Design and Outcome Measures: Nine healthy male volunteers were studied on two occasions, after a hydrocortisone infusion (0.2 mg/kg/min for 14 hours) and a saline infusion, respectively, given in randomized double-blind order. The subjects were studied in the fasting state and after a 75-g glucose drink with an in vivo assessment of femoral adipose tissue blood flow (ATBF) using radioactive xenon washout and of lipolysis and glucose uptake using the arteriovenous difference technique. In a separate study (same infusion design), eight additional healthy male subjects underwent assessment of fasting abdominal ATBF and lipolysis only. Lipolysis was assessed as the net release of nonesterified fatty acids (NEFAs) from femoral and abdominal subcutaneous adipose tissue. Results: Acute hypercortisolemia significantly increased basal and postprandial ATBF in femoral adipose tissue, but the femoral net NEFA release did not change. In abdominal adipose tissue, hypercortisolemia induced substantial increases in basal ATBF and NEFA release. Conclusions: Acute hypercortisolemia induces differential lipolysis and ATBF responses in abdominal and femoral adipose tissue, suggesting depot-specific glucocorticoid effects. Abdominal, but not femoral, adipose tissue contributes to the hypercortisolemia-induced systemic NEFA increase, with likely contributions from other adipose tissue sources and intravascular triglyceride hydrolysis.

scholarly journals Metabolic characteristics of human subcutaneous abdominal adipose tissueafter overnight fast

2012 ◽  
Vol 302 (4) ◽  
pp. E468-E475 ◽  
Author(s):  
Keith N. Frayn ◽  
Sandy M. Humphreys
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Human Adipose Tissue ◽  
Tissue Blood Flow ◽  
Nonesterified Fatty Acids ◽  
Abdominal Adipose Tissue ◽  
Adipose Tissue Metabolism ◽  
Tissue Metabolism ◽  
Subcutaneous Abdominal Adipose Tissue

Subcutaneous abdominal adipose tissue is one of the largest fat depots and contributes the major proportion of circulating nonesterified fatty acids (NEFA). Little is known about aspects of human adipose tissue metabolism in vivo other than lipolysis. Here we collated data from 331 experiments in 255 healthy volunteers over a 23-year period, in which subcutaneous abdominal adipose tissue metabolism was studied by measurements of arterio-venous differences after an overnight fast. NEFA and glycerol were released in a ratio of 2.7:1, different ( P < 0.001) from the value of 3.0 that would indicate no fatty acid re-esterification. Fatty acid re-esterification was 10.2 ± 1.4%. Extraction of triacylglycerol (TG) (fractional extraction 5.7 ± 0.4%) indicated intravascular lipolysis by lipoprotein lipase, and this contributed 21 ± 3% of the glycerol released. Glucose uptake (fractional extraction 2.6 ± 0.3%) was partitioned around 20–25% for provision of glycerol 3-phosphate and 30% into lactate production. There was release of lactate and pyruvate, with extraction of the ketone bodies 3-hydroxybutyrate and acetoacetate, although these were small numerically compared with TG and glucose uptake. NEFA release (expressed per 100 g tissue) correlated inversely with measures of fat mass (e.g., with BMI, rs= −0.24, P < 0.001). We examined within-person variability. Systemic NEFA concentrations, NEFA release, fatty acid re-esterification, and adipose tissue blood flow were all more consistent within than between individuals. This picture of human adipose tissue metabolism in the fasted state should contribute to a greater understanding of adipose tissue physiology and pathophysiology.

Lack of antilipolytic effect of lactate in subcutaneous abdominal adipose tissue during exercise

1999 ◽  
Vol 86 (6) ◽  
pp. 1800-1804 ◽  
Author(s):  
François Trudeau ◽  
Sylvain Bernier ◽  
Isabelle de Glisezinski ◽  
François Crampes ◽  
François Dulac ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Tissue ◽  
Maximal Oxygen Consumption ◽  
Physiological Saline ◽  
Tissue Blood Flow ◽  
Glycerol Concentration ◽  
Abdominal Adipose Tissue ◽  
Glycerol Level ◽  
Good Physical Condition ◽  
Subcutaneous Abdominal Adipose Tissue

The purpose of our study was to evaluate the potential inhibition of adipose tissue mobilization by lactate. Eight male subjects (age, 26.25 ± 1.75 yr) in good physical condition (maximal oxygen uptake, 59.87 ± 2.77 ml ⋅ kg−1 ⋅ min−1; %body fat, 10.15 ± 0.89%) participated in this study. For each subject, two microdialysis probes were inserted into abdominal subcutaneous tissue. Lactate (16 mM) was perfused via one of the probes while physiological saline only was perfused via the other, both at a flow rate of 2.5 μl/min. In both probes, ethanol was also perfused for adipose tissue blood flow estimation. Dialysates were collected every 10 min during rest (30 min), exercise at 50% maximal oxygen consumption (120 min), and recovery (30 min) for the measurement of glycerol concentration. During exercise, glycerol increased significantly in both probes. However, no differences in glycerol level and ethanol extraction were observed between the lactate and control probes. These findings suggest that lactate does not impair subcutaneous abdominal adipose tissue mobilization during exercise.

Increased in vitro fatty acid supply and cellular transport capacities in cold-acclimated ducklings (Cairina moschata)

1998 ◽  
Vol 275 (3) ◽  
pp. R683-R690 ◽  
Author(s):  
Christophe Bénistant ◽  
Claude Duchamp ◽  
Frédérique Cohen-Adad ◽  
Jean-Louis Rouanet ◽  
Hervé Barré
Keyword(s):  
Adipose Tissue ◽  
Gastrocnemius Muscle ◽  
Lipolytic Activity ◽  
Binding Capacity ◽  
Cellular Transport ◽  
Transport Capacity ◽  
Nonesterified Fatty Acids ◽  
Cairina Moschata

In cold-acclimated (CA) birds, lipids play a crucial role in regulatory thermogenesis by acting both as substrates for and activators of thermogenic processes. The capacity to supply lipids to thermogenic tissues, which could limit cold thermogenesis, was assessed in CA ducklings (5 wk old, 4°C) and compared with thermoneutral controls (TN, 25°C). In CA ducklings, basal lipolytic activity of adipose tissue fragments was higher (202 ± 9 vs. 130 ± 14 nmol glycerol released ⋅ 100 mg tissue−1 ⋅ h−1, +55%) than in TN controls, while glucagon had a much higher stimulatory effect (+140 to +500% depending on dose). This was consistent with increased plasma levels of nonesterified fatty acids (FA, +57%) and glycerol (+31%) in vivo. In vitro endothelial lipase activity per organ was higher in CA than in TN ducklings in red gastrocnemius muscle (6.3 ± 0.6 vs. 3.5 ± 0.3 μeq nonesterified FA released per hour, +80%) and liver (+55%). The intracellular FA-binding capacity of (12–18 kDa) proteins was higher in gastrocnemius muscle (+43%) and liver (+74%) from CA ducklings. In gastrocnemius, it was linked to a higher content (21 ± 2 vs. 15 ± 2 μg/mg protein, +37%) of an intracellular 15.4-kDa FA-binding protein. These in vitro results indicate that coordinated increases in FA supply from adipose tissue, cellular uptake of lipoprotein-derived FA, and intracellular FA transport capacity occur in CA ducklings endowed with higher thermogenic capacity and cold endurance.

An in vivo study of the cortisol-cortisone shuttle in subcutaneous abdominal adipose tissue

1999 ◽  
Vol 50 (1) ◽  
pp. 63-68 ◽  
Author(s):  
J. R. Katz ◽  
V. Mohamed-Ali ◽  
P. J. Wood ◽  
J. S. Yudkin ◽  
S. W. Coppack
Keyword(s):  
Adipose Tissue ◽  
In Vivo Study ◽  
Abdominal Adipose Tissue ◽  
Subcutaneous Abdominal Adipose Tissue

Aldosterone blunts the baroreflex response in man

1998 ◽  
Vol 95 (6) ◽  
pp. 687-692 ◽  
Author(s):  
K. M. YEE ◽  
A. D. STRUTHERS
Keyword(s):  
Blood Pressure ◽  
Animal Models ◽  
Sodium Nitroprusside ◽  
Baroreflex Sensitivity ◽  
Crossover Fashion ◽  
Healthy Male ◽  
Double Blind ◽  
Resting Blood Pressure ◽  
Blood Pressure Responses

1. Recent animal evidence suggests that aldosterone, like angiotensin II, may possess detrimental autonomic modulating properties. Aldosterone has been shown to impair the baroreflex response in animal models. This study is designed to test the hypothesis that aldosterone directly attenuates the baroreflex in vivo in man. 2. Fourteen healthy male volunteers [mean age (S.D.) 25 (9) years] received intravenous d-aldosterone (12 pmol·min-1·kg-1) and 5% dextrose (vehicle) in a double-blind crossover fashion, co-infused with incremental doses of intravenous phenylephrine and sodium nitroprusside. Aldosterone had no significant effect on resting blood pressure, heart rate or baroreflex response to sodium nitroprusside. However, reflex responses to phenylephrine were impaired with aldosterone (P< 0.01) while blood pressure responses were unaltered. Baroreflex sensitivity was significantly blunted in the aldosterone group [8.36±2.19 versus 10.12±2.27 ms/mmHg; P< 0.04]. 3. This study confirms previous observations from animal models that aldosterone impairs the baroreflex response. High aldosterone levels may contribute to the baroreflex dysfunction in cardiovascular diseases such as hypertension and heart failure.

scholarly journals Effects of Hypo- and Hyperthyroidism on Noradrenergic Activity and Glycerol Concentrations in Human Subcutaneous Abdominal Adipose Tissue Assessed with Microdialysis

2003 ◽  
Vol 88 (12) ◽  
pp. 5605-5608 ◽  
Author(s):  
Martin Haluzik ◽  
Jara Nedvidkova ◽  
Vladimir Bartak ◽  
Ivana Dostalova ◽  
Petr Vlcek ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormones ◽  
Relative Magnitude ◽  
In Vivo Microdialysis ◽  
Abdominal Adipose Tissue ◽  
Subcutaneous Abdominal Adipose Tissue ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients ◽  
Tissue Norepinephrine

Abstract Thyroid hormones play a major role in lipid metabolism. However, whether they directly affect lipolysis locally in the adipose tissue remains unknown. Therefore, we measured abdominal sc adipose tissue norepinephrine (NE), basal, and isoprenaline-stimulated lipolysis in 12 hypothyroid patients (HYPO), six hyperthyroid patients (HYPER), and 12 healthy controls by in vivo microdialysis. Adipose tissue NE was decreased in HYPO and increased in HYPER compared with controls (90.4 ± 2.9 and 458.0 ± 69.1 vs. 294.9 ± 19.5 pmol/liter, P &lt; 0.01). Similarly, basal lipolysis, assessed by glycerol assay, was lower in HYPO and higher in HYPER than in controls (88.2 ± 9.9 and 566.0 ± 42.0 vs. 214.3 ± 5.1 μmol/liter P &lt; 0.01). The relative magnitude of isoprenaline-induced glycerol increase was smaller in HYPO (39 ± 19.4%, P &lt; 0.05 vs. basal) and higher in HYPER (277 ± 30.4%, P &lt; 0.01) than in controls (117 ± 5.6%, P &lt; 0.01). The corresponding changes in NE after isoprenaline stimulation were as follows: 120 ± 9.2% (P &lt; 0.05), 503 ± 113% (P &lt; 0.01), and 267 ± 17.2 (P &lt; 0.01). In summary, by affecting local NE levels and adrenergic postreceptor signaling, thyroid hormones may influence the lipolysis rate in the abdominal sc adipose tissue.

scholarly journals Enhanced glycogen metabolism in adipose tissue decreases triglyceride mobilization

2010 ◽  
Vol 299 (1) ◽  
pp. E117-E125 ◽  
Author(s):  
Kathleen R. Markan ◽  
Michael J. Jurczak ◽  
Margaret B. Allison ◽  
Honggang Ye ◽  
Maria M. Sutanto ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Lactate Production ◽  
Transgenic Animals ◽  
Whole Body ◽  
Nonesterified Fatty Acids ◽  
Transgenic Mouse Line ◽  
Whole Body Metabolism

Adipose tissue is a primary site for lipid storage containing trace amounts of glycogen. However, refeeding after a prolonged partial fast produces a marked transient spike in adipose glycogen, which dissipates in coordination with the initiation of lipid resynthesis. To further study the potential interplay between glycogen and lipid metabolism in adipose tissue, the aP2-PTG transgenic mouse line was utilized since it contains a 100- to 400-fold elevation of adipocyte glycogen levels that are mobilized upon fasting. To determine the fate of the released glucose 1-phosphate, a series of metabolic measurements were made. Basal and isoproterenol-stimulated lactate production in vitro was significantly increased in adipose tissue from transgenic animals. In parallel, basal and isoproterenol-induced release of nonesterified fatty acids (NEFAs) was significantly reduced in transgenic adipose tissue vs. control. Interestingly, glycerol release was unchanged between the genotypes, suggesting that enhanced triglyceride resynthesis was occurring in the transgenic tissue. Qualitatively similar results for NEFA and glycerol levels between wild-type and transgenic animals were obtained in vivo during fasting. Additionally, the physiological upregulation of the phospho enolpyruvate carboxykinase cytosolic isoform (PEPCK-C) expression in adipose upon fasting was significantly blunted in transgenic mice. No changes in whole body metabolism were detected through indirect calorimetry. Yet weight loss following a weight gain/loss protocol was significantly impeded in the transgenic animals, indicating a further impairment in triglyceride mobilization. Cumulatively, these results support the notion that the adipocyte possesses a set point for glycogen, which is altered in response to nutritional cues, enabling the coordination of adipose glycogen turnover with lipid metabolism.

Uptake of glucose and release of fatty acids and glycerol by rat brown adipose tissue in vivo

1986 ◽  
Vol 64 (5) ◽  
pp. 609-614 ◽  
Author(s):  
Stephanie W. Y. Ma ◽  
David O. Foster
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Tissue Blood Flow ◽  
Glycerol Release ◽  
Maximal Stimulation ◽  
Brown Adipose ◽  
Lactate And Pyruvate

The net in vivo uptake or release of free fatty acids glycerol, glucose, lactate, and pyruvate by the interscapular brown adipose tissue (IBAT) of barbital-anesthetized, cold-acclimated rats was determined from measurements of plasma arteriovenous concentration differences across IBAT and tissue blood flow. Measurements were made without stimulation of the tissue and also during submaximal and maximal stimulation by infused noradrenaline (NA), the physiological activator of BAT thermogenesis. There was no appreciable uptake of glucose or release of fatty acids and glycerol by the nonstimulated tissue. At both levels of stimulation there was significant uptake of glucose (1.7 and 2.0 μmol/min) and release of glycerol (0.9 and 1.2 μmol/min), but only at maximal stimulation was there significant release of fatty acids (1.9 μmol/min). Release of lactate and pyruvate accounted for 33% of the glucose taken up at submaximal stimulation and 88% at maximal stimulation. By calculation, the remainder of the glucose taken up was sufficient to have fueled about 12% of the thermogenesis at submaximal stimulation, but only about 2% at maximal stimulation. As estimated from the rate of glycerol release, the rate of triglyceride hydrolysis was sufficient at submaximal stimulation to fuel IBAT thermogenesis entirely with the resulting fatty acids, but it was not sufficient to do so at maximal stimulation when some of the fatty acid was exported. It is suggested that at maximal NA-induced thermogenesis a portion of lipolysis proceeded only to the level of mono- and di-glycerides with the result that glycerol release did not fully reflect the rate of fatty acid formation. Both in absolute terms and in relation to the export of glycerol the in vivo export of fatty acids from the adipocytes of IBAT was much less than is observed with brown adipocytes in vitro.

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