scholarly journals Changes in the sensitivity to glucagon of lipolysis in adipocytes from pregnant and lactating rats

1988 ◽  
Vol 254 (3) ◽  
pp. 661-665 ◽  
Author(s):  
V A Zammit
Keyword(s):  
Adipose Tissue ◽  
The Other ◽  
High Concentration ◽  
Response Curves ◽  
Pregnant Rats ◽  
Adipose Tissue Lipolysis ◽  
The Right ◽  
Peak Lactation ◽  
Stimulation Of

1. Rates of lipolysis were measured at different concentrations of glucagon in adipocytes prepared from parametrial adipose tissue of fed or starved rats in different reproductive states. All experiments were performed in the presence of a high concentration of adenosine deaminase (1 unit/ml). 2. Maximal rates of lipolysis (elicited by 25 nM-glucagon in each instance) were higher in adipocytes from peak-lactating rats than those from pregnant animals in both the fed and starved states. 3. Of adipocytes from fed animals, those from peak-lactating rats were the most sensitive to glucagon, whereas those from late-pregnant and early-lactating rats were 1-2 orders of magnitude less sensitive. 4. Adipocytes from 24 h-starved rats showed a much smaller stimulation of lipolysis by glucagon, making the assessment of sensitivity difficult. Therefore, rates of lipolysis were also measured in the presence of a maximally anti-lipolytic dose of insulin. The presence of insulin did not alter the relative sensitivities to glucagon of adipocytes from fed animals in different reproductive states, although all dose-response curves were shifted to the right. When lipolysis in adipocytes from starved animals was measured in the presence of insulin, it became evident that starvation for 24 h markedly increased the sensitivity of adipocytes from late-pregnant rats to glucagon, but did not affect that of cells from animals in the other reproductive states. 5. It is concluded that the large changes in sensitivity to glucagon that occurred during the reproductive cycle may enable the modulation of adipose-tissue lipolysis in vivo to satisfy the different metabolic requirements of the animal in the transition from pregnancy to peak lactation.

Regulation of lipolysis by somatotropin: functional alteration of adrenergic and adenosine signaling in bovine adipose tissue

1997 ◽  
Vol 152 (3) ◽  
pp. 465-475 ◽  
Author(s):  
K L Houseknecht ◽  
D E Bauman
Keyword(s):  
Adipose Tissue ◽  
Signaling Proteins ◽  
Heterotrimeric G Proteins ◽  
Adrenergic Stimulation ◽  
Cellular Mechanisms ◽  
Lactating Cows ◽  
Adipose Tissue Lipolysis ◽  
Stimulation Of

To investigate the cellular mechanisms of somatotropin (ST) action on adipose tissue lipolysis, experiments were conducted using adipose tissue taken from lactating cows treated with excipient or ST (40 mg/day). Stimulation of lipolysis in vitro by the effectors isoproterenol with or without adenosine deaminase, dibutyryl cAMP with or without isobutylmethylxanthine, and forskolin was not altered by ST treatment. Conversely, the response to the antilipolytic effector, phenylisopropyladenosine (PIA), was significantly reduced in adipose tissue explants from ST or fasted cows. The different responses to adrenergic-stimulating agents (in vivo) and PIA (in vitro) were not due to differences in the abundance of α, β or γ subunits of the stimulatory (Gs) and inhibitory (Gi) subunits of the heterotrimeric G-proteins which bind to the β-adrenergic and adenosine receptors respectively. However, the functionality of Gi proteins, as assessed by their ability to be ADP-ribosylated by pertussis toxin, was significantly reduced in ST-treated but not fasted cows. These data highlight differential regulation of signaling proteins by ST and fasting, both of which result in enhanced in vivo response to adrenergic stimulation of lipolysis. Journal of Endocrinology (1997) 152, 465–475

Acute metabolic effects of adrenergic agents in swine

1987 ◽  
Vol 252 (1) ◽  
pp. E85-E95 ◽  
Author(s):  
H. J. Mersmann
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Metabolic Effects ◽  
Adipose Tissue Lipolysis ◽  
Beta 2 ◽  
Stimulation Of

A pig model in vivo was used to confirm the unique specificity for stimulation of porcine adipose tissue lipolysis by norepinephrine analogues in vitro. Plasma free fatty acid and blood glycerol concentrations were monitored as probable indicators of adipose tissue lipolysis. Plasma glucose and lactate concentrations, blood pressure, and heart rate were monitored also. Norepinephrine analogues were infused intravenously. Several compounds, classified as either beta 1- or beta 2-adrenergic agonists, that stimulated lipolysis in vitro also increased plasma free fatty acid and blood glycerol concentrations in vivo. Tazolol (beta 1) and quinterenol (beta 2) did not stimulate lipolysis in vitro and likewise did not elevate plasma free fatty acid or blood glycerol concentrations in vivo. Clenbuterol and zinterol did not stimulate lipolysis in vitro but elevated plasma free fatty acid concentrations in vivo, implying indirect effects. Isoproterenol stimulation of plasma free fatty acid and blood glycerol concentrations in vivo was antagonized by propranolol, implying the beta-adrenergic nature of the receptors. Infusion of purported beta 1- and beta 2-adrenergic antagonists suggested control of lipolysis in vivo predominantly by beta 1-adrenergic receptors; however, because the results in vitro do not indicate this specificity, differential pharmacodynamics of the antagonists are suggested rather than designation of receptor subtypes. There was no evidence for alpha-adrenergic mediated inhibition of adipose tissue lipolysis in vivo, confirming observations in vitro.

scholarly journals Pharmacologically mechanistic basis for the traditional uses of Rumex acetosa in gut motility disorders and emesis

2015 ◽  
Vol 10 (3) ◽  
pp. 548 ◽  
Author(s):  
Musaddique Hussain ◽  
Shahid Masood Raza ◽  
Khalid Hussain Janbaz
Keyword(s):  
Rumex Acetosa ◽  
Response Curves ◽  
Motility Disorders ◽  
Traditional Uses ◽  
Antiemetic Activity ◽  
Rabbit Jejunum ◽  
Mechanistic Basis ◽  
The Right

<p class="Abstract"><em>In vitro</em> and<em> in vivo</em> studies were undertaken to evaluate the pharmacologically mechanistic background to validate the traditional uses of <em>Rumex acetosa</em> in the treatment of emesis and gastrointestinal motility disorders such as constipation and diarrhea. In rabbit jejunum preparation, methanolic extract of <em>R. acetosa</em> (0.01-1.0 mg/mL) caused a transient spasmogenic effect, followed by the spasmolytic effect (3-10 mg/mL). In presence of atropine, spasmogenic effect was blocked while spasmolytic effect was emerged, suggesting that spasmogenic effect was mediated through activation of muscarinic receptors. Extract inhibited the K<sup>+ </sup>(80 mM)-induced contraction, suggesting Ca<sup>2+</sup>-cha-nnel blockade, which was further confirmed when pretreatment of tissue with extract shifted the Ca<sup>2+ </sup>concentration-response curves to the right, similarly as verapamil.<em> R. acetosa</em> also exhibited the significant antiemetic activity (p&lt;0.05) against different emetogenic stimuli, when compared with chlorpromazine. This study confirms the presence of gut modulator (spasmogenic and spasmolytic) and antiemetic activates, validating its traditional uses.</p><p> </p>

Control of brown adipose tissue lipolysis and respiration by adenosine

1983 ◽  
Vol 245 (6) ◽  
pp. E555-E559 ◽  
Author(s):  
D. Szillat ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Palmitic Acid ◽  
Brown Adipose Tissue ◽  
Brown Adipocyte ◽  
Tissue Respiration ◽  
Dibutyryl Cyclic Amp ◽  
Response Curves ◽  
Brown Adipose ◽  
Stimulation Of

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

Lipolytic responsiveness to epinephrine in nondiabetic and diabetic humans

1997 ◽  
Vol 272 (6) ◽  
pp. E1130-E1135 ◽  
Author(s):  
G. D. Divertie ◽  
M. D. Jensen ◽  
P. E. Cryer ◽  
J. M. Miles
Keyword(s):  
Adipose Tissue ◽  
Insulin Dependent Diabetes ◽  
Response Curves ◽  
Epinephrine Infusion ◽  
Hormone Levels ◽  
Control Subjects ◽  
Insulin Dependent ◽  
Adipose Tissue Lipolysis ◽  
Plasma Hormone ◽  
Beta Hydroxybutyrate

To determine whether the sensitivity of adipose tissue lipolysis to catecholamines is increased in poorly controlled insulin-dependent diabetes, the lipolytic response to epinephrine was measured in seven nondiabetic volunteers and seven poorly controlled diabetic subjects with use of [1-(14)C]palmitate as a tracer. Subjects received sequential 1-h infusions of epinephrine, which produced epinephrine concentrations of approximately 1,000, approximately 1,750, approximately 3,500, and approximately 6,000 pmol/l. A pancreatic clamp was used to maintain constant plasma hormone levels. Concentration-response curves were constructed for each subject from the integrated lipolytic response during each epinephrine infusion. There was no difference in maximal lipolytic response (117 +/- 19 vs. 152 +/- 11 mumol.kg-1.h-1) or in maximally effective (3,171 +/- 267 vs. 3,357 +/- 349 pmol/l) or half-maximally effective (1,081 +/- 109 vs. 1,015 +/- 120 pmol/l) epinephrine concentrations between nondiabetic and diabetic subjects, respectively (all P = NS). In control subjects, maximum beta-hydroxybutyrate concentrations were achieved at lower epinephrine concentrations than those required for a maximum lipolytic effect. Thus, under pancreatic clamp conditions, the lipolytic response to epinephrine in nondiabetic and diabetic subjects was similar.

scholarly journals Insulin-like stimulation of cardiac fuel metabolism by physiological levels of glucagon: involvement of PI3K but not cAMP

2008 ◽  
Vol 295 (1) ◽  
pp. E155-E161 ◽  
Author(s):  
Julie A. Harney ◽  
Robert L. Rodgers
Keyword(s):  
Left Ventricular Pressure ◽  
Adenosine Monophosphate ◽  
Left Ventricular ◽  
Glycolytic Flux ◽  
Blood Levels ◽  
Response Curves ◽  
Fuel Metabolism ◽  
Camp Levels ◽  
Stimulation Of

At concentrations around 10−9 M or higher, glucagon increases cardiac contractility by activating adenylate cyclase/cyclic adenosine monophosphate (AC/cAMP). However, blood levels in vivo, in rats or humans, rarely exceed 10−10 M. We investigated whether physiological concentrations of glucagon, not sufficient to increase contractility or ventricular cAMP levels, can influence fuel metabolism in perfused working rat hearts. Two distinct glucagon dose-response curves emerged. One was an expected increase in left ventricular pressure (LVP) occurring between 10−9.5 and 10−8 M. The elevations in both LVP and ventricular cAMP levels produced by the maximal concentration (10−8 M) were blocked by the AC inhibitor NKY80 (20 μM). The other curve, generated at much lower glucagon concentrations and overlapping normal blood levels (10−11 to 10−10 M), consisted of a dose-dependent and marked stimulation of glycolysis with no change in LVP. In addition to stimulating glycolysis, glucagon (10−10 M) also increased glucose oxidation and suppressed palmitate oxidation, mimicking known effects of insulin, without altering ventricular cAMP levels. Elevations in glycolytic flux produced by either glucagon (10−10 M) or insulin (4 × 10−10 M) were abolished by the phosphoinositide 3-kinase (PI3K) inhibitor LY-294002 (10 μM) but not significantly affected by NKY80. Glucagon also, like insulin, enhanced the phosphorylation of Akt/PKB, a downstream target of PI3K, and these effects were also abolished by LY-294002. The results are consistent with the hypothesis that physiological levels of glucagon produce insulin-like increases in cardiac glucose utilization in vivo through activation of PI3K and not AC/cAMP.

scholarly journals Effect of denture surface glazing on denture plaque formation

2005 ◽  
Vol 16 (2) ◽  
pp. 129-134 ◽  
Author(s):  
Newton Sesma ◽  
Dalva Cruz Laganá ◽  
Susana Morimoto ◽  
Carlos Gil
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Bacterial Colonization ◽  
Plaque Formation ◽  
The Other ◽  
Bacterial Plaque ◽  
The Right ◽  
Clinical Experiment ◽  
Scanning Electron

This study evaluated, in vivo, the efficacy of a denture glazing material (Palaseal) in modifying plaque colonization of dentures. Ten subjects were selected and received maxillary temporary partial removable dentures, with complete acrylic palatal coverage. The right half of the fitting surface of the denture bases were glazed with Palaseal, whereas the other half was not glazed. One month after insertion, two fragments of the resin base of all dentures were removed (one from the glazed side and another from the non-glazed side). These samples were prepared and examined by scanning electron microscopy. Three months after insertion, other fragments were obtained and analyzed. Microscopic observation at 1 month revealed that, for all patients, the plaque film was thinner on the treated side in comparison to the non-treated side. However, at the 3-month evaluation, some areas of the glaze showed cracking, and both glazed and non-glazed sides were covered by a dense bacterial plaque film. In conclusion, the findings of this clinical experiment showed that glazing denture's fitting surface did not prevent bacterial colonization, but favored plaque removal while the glaze layer remained intact. After three months, glaze cracks created microretentive areas that increased plaque accumulation.

scholarly journals Impaired noradrenaline-induced lipolysis in white fat of aP2-Ucp1 transgenic mice is associated with changes in G-protein levels

2002 ◽  
Vol 364 (2) ◽  
pp. 369-376 ◽  
Author(s):  
Pavel FLACHS ◽  
JiŘí NOVOTNÝ ◽  
Filip BAUMRUK ◽  
Kristina BARDOVÁ ◽  
Lenka BOUŘOVÁ ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Transgenic Mice ◽  
G Protein ◽  
Energy Status ◽  
Α Subunit ◽  
Fat Depots ◽  
Ucp1 Expression ◽  
White Fat ◽  
Stimulation Of

In vitro experiments suggest that stimulation of lipolysis by catecholamines in adipocytes depends on the energy status of these cells. We tested whether mitochondrial uncoupling proteins (UCPs) that control the efficiency of ATP production could affect lipolysis and noradrenaline signalling in white fat in vivo. The lipolytic effect of noradrenaline was lowered by ectopic UCP1 in white adipocytes of aP2-Ucp1 transgenic mice, overexpressing the UCP1 gene from the aP2 gene promoter, reflecting the magnitude of UCP1 expression, the impaired stimulation of cAMP levels by noradrenaline and the reduction of the ATP/ADP ratio in different fat depots. Thus only subcutaneous but not epididymal fat was affected. UCP1 also down-regulated the expression of hormone-sensitive lipase and lowered its activity, and altered the expression of trimeric G-proteins in adipocytes. The adipose tissue content of the stimulatory G-protein α subunit was increased while that of the inhibitory G-protein α subunits decreased in response to UCP1 expression. Our results support the idea that the energy status of cells, and the ATP/ADP ratio in particular, modulates the lipolytic effects of noradrenaline in adipose tissue in vivo. They also demonstrate changes at the G-protein level that tend to overcome the reduction of lipolysis when ATP level in adipocytes is low. Therefore, respiratory uncoupling may exert a broad effect on hormonal signalling in adipocytes.

Studies on antihypertensive and antispasmodic activities of Andropogon muricatus Retz.This article is one of a selection of papers published in this special issue (part 1 of 2) on the Safety and Efficacy of Natural Health Products.

2007 ◽  
Vol 85 (9) ◽  
pp. 911-917 ◽  
Author(s):  
Anwar H. Gilani ◽  
Abdul J. Shah ◽  
Khalid H. Janbaz ◽  
Shahida P. Ahmed ◽  
Muhammad N. Ghayur
Keyword(s):  
Calcium Channel ◽  
Rabbit Aorta ◽  
Natural Health Products ◽  
Response Curves ◽  
Medicinal Uses ◽  
Health Products ◽  
Rabbit Jejunum ◽  
The Right

The aqueous-methanolic crude extract of Andropogon muricatus (Am.Cr) was investigated pharmacologically to determine some of its medicinal uses in cardiovascular and gastrointestinal disorders. A series of in vivo and in vitro studies were conducted to evaluate dose-dependent effects of Am.Cr on mean arterial pressure (MAP), cardiac and vascular contractions, and to further investigate the potential mechanism of action. Intravenous administration of Am.Cr (10–50 mg/kg) caused a fall (18%–56%) in MAP in normotensive rats under anesthesia. When tested in isolated guinea pig atria, Am.Cr (0.03–5.0 mg/mL) exhibited a cardiodepressant effect on the rate and force of spontaneous contractions. In isolated rabbit aorta, Am.Cr caused inhibition of K+ (80 mmol/L)-induced contractions at a lower concentration than of phenylephrine. In isolated rabbit jejunum preparations, Am.Cr (0.01–0.10 mg/mL) caused relaxation of spontaneous and high K+ (80 mmol/L)-induced contractions, suggesting that the spasmolytic effect is mediated possibly through calcium channel blockade (CCB). The CCB activity was confirmed when pretreatment of the tissue with Am.Cr (0.03–0.1 mg/mL) shifted the Ca2+ dose–response curves to the right, similar to that caused by verapamil. These data indicate that the blood pressure-lowering and spasmolytic effects of Am.Cr are mediated possibly through a calcium channel blocking activity. Phytochemical screening of Am.Cr revealed the presence of phenols, saponins, tannins, and terpenes, which may be responsible for the observed vasodilator, cardiodepressant, and antispasmodic activities. This study shows potential with respect to its medicinal use in cardiovascular and gut disorders.

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