Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Triiodo-L-thyronine (T(3)) added in vitro to fat pads from normal, or propylthiouracil-treated rats enhanced the rate of release of glycerol and free fatty acids (FFA) in the presence of epinephrine. An effect of T(3) was also demonstrated in the presence of adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone, or glucagon in studies with tissue from normal rats. The minimal effective concentration of T(3) was approximately 2.5 x 10(-5) mole/liter for intact fat pads and 3 x 10(-6) mole/liter for fat cells. With fat pads from propylthiouracil-treated rats the effect of T(3) was not apparent until the 3rd hr of incubation. Enhancement of epinephrine-stimulated lipolysis by T(3) was evident during the 1st hr of incubation of fat pads from normal rats, and fat cells responded almost immediately to the presence of T(3). When added alone or in the presence of theophylline, 3',5'-adenosine monophosphate or its dibutyryl derivative, T(3) had little or no effect on lipolysis. The effect of T(3) was observed with or without glucose in the medium, and was not inhibited by cycloheximide or actinomycin D. It did not persist when tissues, after incubation in the presence of T(3) were transferred to medium without T(3). No effect of T(3) on glucose uptake in the presence of epinephrine, ACTH, or insulin was demonstrated.
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PMID:An in vitro effect of triiodothyronine on rat adipose tissue. 429 92

A specific and sensitive assay for determining the binding of adrenocorticotropin (ACTH) to isolated rat adipocytes has been developed and utilized to study the effect of glucocorticoids on ACTH receptor. Measurement of the binding of tritiated ACTH (spec. act. 90 Ci/mmol) to adipocytes isolated from normal, adrenalectomized, and adrenalectomized dexamethasone-treated rats indicated that there are no differences among these three populations in either the magnitude or the affinity of the binding reaction. The binding interaction was found to be of high affinity (Kd = 5.23 + 1.92 . 10(-9) M and paralleled closely the stimulation of lipolysis (Km = 2.09 +/- 0.35 . 10(-9) M. About 16,300 receptors were calculated to be presented per adipocyte. Hormone-induced cyclic 3',5'-adenosine monophosphate production remained intact after adrenalectomy, thereby confirming that receptors are not lost during steroid deprivation. The lipolytic response did, however, become less sensitive to both ACTH and epinephrine following adrenalectomy. Pre-treatment of adrenalectomized rats with dexamethasone resulted in an increase in basal and hormone-stimulated levels of cyclic AMP and glycerol production to super-normal values. In adipocyte ghost preparations, ACTH and epinephrine sensitive adenylate cyclase activity was not decreased by adrenalectomy and dexamethasone administration did not result in a selective enhancement of ACTH sensitive adenylate cyclase activity. Our results indicate that glucocorticoids do not cause their permissive effects by specific regulation of the ACTH receptor on the adipocyte.
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PMID:The effect of glucocorticoids on adipocyte corticotropin receptors and adipocyte responses. 626 Feb 29

We studied the effects of adrenocorticotropin (ACTH) and cycloheximide on adrenal enzymes involved in phosphatidate synthesis. Treatment of rats in vivo with ACTH induced a rapid increase in phosphatide synthesis from diglyceride and ATP in adrenal homogenates, and cycloheximide treatment prevented this increase if given before ACTH and rapidly reversed the increase if given after ACTH. The stimulatory effect of ACTH appeared to be largely due to an increase in diglyceride substrate, as kinase activity was not altered. The inhibitory effect of cycloheximide, on the other hand, appeared to be due to a decrease in diglyceride kinase activity. Neither ACTH nor cycloheximide treatment had any effect on the activity of glycerol-3'-phosphate acyltransferase or phosphatidate phosphatase. Our findings suggest that (a) ACTH increases the flow of phospholipid (and their levels) throughout the entire circular pathway, i.e., phosphatidate leads to CDP-diacylglycerol leads to inositides leads to diglycerides leads to phosphatidate, and (b) a labile protein may serve to allow entry into a recycling of diglyceride in this pathway. In addition, since cycloheximide blocked carbachol-induced increases in pancreatic and salivary glandular phosphatidate synthesis resulting from phosphatidylinositol hydrolysis and consequent diglyceride generation, the putative labile protein may have widespread importance.
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PMID:Effects of adrenocorticotropin and cycloheximide on adrenal diglyceride kinase. 627 34

Triphenylmethylphosphonium (TPMP+) partitions into the mitochondrial and cytosolic compartments in the rat white adipocyte in a potential-dependent fashion. The relationship between [3H]TPMP+ distribution, intracellular cAMP generation and lipolysis in response to hormones and cAMP-mimetic compounds was examined. Half-maximal [3H]TPMP+ efflux and glycerol release were produced by 15 and 9 nM adrenocorticotropin, 170 and 110 nM 1-epinephrine, 70 and 27 microM isobutylmethylxanthine and 800 and 750 microM dibutyryl cAMP, respectively. Hormone-stimulated cAMP generation was also correlated with [3H]TPMP+ efflux and lipolysis in terms of concentration dependency. In kinetic experiments, glycerol release and [3H]TPMP+ efflux in response to adrenocorticotropin or cholera toxin proceeded over a similar time course, whereas an earlier rise in cAMP generation was detected. The depolarizing effect of lipolytic compounds was localized to the mitochondrial compartment. When cells were incubated in elevated-[K+]0 buffer, the stimulatory effect of dibutyryl cAMP on [3H]TPMP+ efflux and lipolysis persisted, suggesting that maintenance of the plasma membrane potential is not critical for demonstration of these responses. When the extracellular concentration of serum albumin, which provides binding sites for free fatty acids, was increased from 1 to 3%, an increase in glycerol release and a decrease in [3H]TPMP+ efflux was observed. We suggest that intracellular free fatty acid accumulation in response to lipolytic agents causes dissipation of the mitochondrial membrane potential and efflux of [3H]TPMP+ from the organelle and cell.
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PMID:Triphenylmethylphosphonium cation distribution as a measure of hormone-induced alterations in white adipocyte membrane potential. 628 74

The hypothesis that lipolytic hormones reduce the mitochondrial electrical potential in rat white adipocytes via free fatty acids (FFA) was examined. Hormonal effects on plasma and mitochondrial membrane potentials were evaluated with [3H]triphenylmethylphosphonium (TPMP+) and 86Rb+. FFA generation was controlled by varying medium albumin concentrations. In 4.0% albumin buffer, adrenocorticotropin or l-epinephrine increased intracellular FFAs, produced cellular TPMP+ efflux, ATP depletion, release of FFAs and glycerol, and no change in 86Rb+ distribution. In 0.5% albumin buffer, greater intracellular FFA accumulation accompanied greater TPMP+ and ATP depletion, significant loss of cell-associated 86Rb+, and a concomitant inhibition of FFA and glycerol release. Exogenous addition of FFAs mimicked the effect of hormones on adipocyte TPMP+ distribution. TPMP+ and 86Rb+ uptake into adipocyte "ghosts" were unaffected by hormones. We suggest that mitochondrial membrane depolarization is a metabolic response to hormones via FFA accumulation by white adipocytes. The additional hormonal effects that were observed in 0.5% albumin buffer may be related to inhibition of lipolysis secondary to intracellular ATP depletion.
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PMID:Hormones modulate adipocyte membrane potential ATP and lipolysis via free fatty acids. 631 Oct 25

Synthetic [125I]-Tyr23, Phe2, Nle4-adrenocorticotropin (ACTH)-(1-38) [( 125I]-ACTH analog) with full biological potency and near theoretical specific radioactivity (1800 +/- 75 Ci/mmol) was used to investigate ACTH receptors on isolated rat adipocytes derived from 42-day-old rats. Binding to adipocytes was studied in the presence of 1% bovine serum albumin (BSA) as well as 4% BSA. The interaction of the [125I]-ACTH analog with adipocytes was highly specific, rapid, saturable, and reversible. Scatchard analysis of the binding data obtained in medium containing 1% BSA revealed a single class of binding sites with an apparent KD = 170 +/- 11.9 pM. Competition experiments with unlabeled ACTH also yielded a comparable value for the apparent KD (143 +/- 16.5 pM). The number of receptors per adipocyte was quite low (521-841/cell). The stimulation of lipolysis by ACTH was closely correlated with the binding, the apparent Km being 145-177 pM. At a concentration of 4% BSA in the incubation medium, the binding curve was shifted significantly to the right (apparent KD = 446 +/- 77 pM) and the binding capacity was also significantly enhanced (1663 +/- 208/cell) without any change in the apparent Km for glycerol release (187 +/- 7.1 pM).
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PMID:Studies of corticotropin receptors on rat adipocytes. 631 87

beta-endorphin stimulates lipolysis in vitro in isolated fat cells of the rabbit. To exclude effects of collagenases and local proteases we investigated the effect of beta-endorphin on glycerol, free fatty acids and glucose plasma levels in the rabbit with and without naloxone. beta-endorphin increased free fatty acids and glycerol while glucose remained unaffected. The increase of glycerol and free fatty acids could be blocked by naloxone, suggesting the involvement of different receptors.
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PMID:beta-endorphin stimulates in vivo lipolysis in the rabbit. 631 25

Inhibitors of protein synthesis, cycloheximide and puromycin, blocked ACTH (adrenocorticotropin)-induced increases in phospholipid mass, including phosphatidylinositol, but paradoxically increase 32P-labelling (but not [3H]glycerol-labelling) therein. Cycloheximide also provoked an initial rapid decrease in 32P-prelabelled phospholipids, followed by an increase in [32P]Pi incorporation. These effects of cycloheximide and puromycin occurred in ACTH-treated (but not in control) cells. It appears that inhibition of protein synthesis during ACTH action provokes an increase in phospholipid degradation, followed by partial resynthesis of the phospholipid head groups.
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PMID:Apparent increases in phospholipid degradation and turnover during combined treatment with protein synthesis inhibitors and adrenocorticotropin. 632 70

beta-lipotropin stimulates lipolysis in the rabbit in a dose dependent manner. Besides glycerol and free fatty acid release a significant increase of betahydroxybutyrate as well as of acetoacetate was observed while pyruvate decreased significantly. Glucose and lactate levels remained unchanged. Our data suggest that lipolysis induced by beta-LPH and its effect on ketogenesis is more important than the actual plasma concentration of insulin.
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PMID:beta-lipotropin increases ketone body plasma concentration in rabbits. 671 61

Group III and IV muscle afferents are active during exercise and relay information from mechano- and metaboreceptors in muscle. We hypothesized that these afferents participate in the regulation of endocrine and metabolic adjustments to exercise. Muscle branches of the femoral nerves were electrically stimulated in 10 anesthetized and paralyzed cats at 3, 20, and 140 times motor threshold, for 10 min at each intensity, recruiting group III afferents at 20 times motor threshold and group III and IV afferents at 140 times motor threshold. Six cats were not stimulated but were otherwise treated as stimulated cats. [3-3H]glucose was infused intravenously, and arterial blood was sampled for analysis of substrates and hormones. Three times motor threshold stimulation induced no changes in measured metabolic parameters. Twenty times motor threshold stimulation elicited increases (P < 0.05 vs. control) in glucose production (8.2 +/- 1.8 mumol.min-1.kg-1) and plasma glucose (0.29 +/- 0.07 mmol/l) and adrenocorticotropic hormone (ACTH; 35 +/- 12 pg/ml). Stimulation at 140 times motor threshold elicited increases (P < 0.05 vs. control) in glucose production (10.2 +/- 5.4 mumol.min-1.kg-1), plasma glucose (0.53 +/- 0.10 mmol/l), ACTH (94 +/- 28 pg/ml), beta-endorphin (17 +/- 6 pg/ml), and Met-enkephalin (15 +/- 2 pg/ml) and decreases (P < 0.05 vs. control) in insulin (0.65 +/- 0.14 microU/ml). Glycerol and glucagon did not change with stimulations. The findings provide evidence for a reflex control from muscle of hormone secretion and mobilization of glucose during exercise.
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PMID:Reflex control of glucoregulatory exercise responses by group III and IV muscle afferents. 816 Aug 77


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