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Results for “Pro-Opiomelanocortin”

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At least 649 records · Page 36Linked to original sources
PubMed1988

[ACTH-secreting tumors. Deregulation of the proopiomelanocortin gene and alterations in processing].

ACTH is produced by proteolysis of a polypeptide precursor, proopiomelanocortin (or POMC). Various POMC-derived peptides are cosecreted with ACTH. Analysis of the ACTH--and its "satellite" peptides--molecular forms establishes the POMC "maturation profile" in different tissues. This profile is identical in normal and tumoral pituitaries (Cushing's disease and/or Nelson's syndrome). It is often altered in non-pituitary tumors responsible for the ectopic ACTH syndrome: abnormal peptides may be generated (CLIP h beta MSH5-22) which can be detected in blood. Analysis of POMC gene transcription in pituitary tumors shows no abnormality. In some non-pituitary tumors the activation of upstream promoters up to 369 nucleotides from the normal (pituitary) transcription initiation site can be shown. In normal non-pituitary tissues a third type of transcription is observed generating a short and probably non-functional messenger RNA limited to a portion of the gene non-coding region.

Adrenal Gland Neoplasms↗
PubMed1988

Increased pro-opiomelanocortin-derived peptide release in myotonic dystrophy.

The response of plasma immunoreactive (IR)-ACTH, IR-beta-endorphin (beta-END) and IR-cortisol to insulin-induced hypoglycaemia, an acute stimulus to the pituitary corticotrophs through the central nervous system, and to synthetic ovine corticotrophin-releasing hormone (CRH), a direct corticotroph stimulator, were studied in normal males and males with myotonic dystrophy. Myotonics had an increased IR-ACTH and IR-beta-END response to hypoglycaemia and an increased IR-ACTH response to CRH compared with normals. Plasma IR-cortisol response were not different in either group of subjects to both stimuli. This neuroendocrine abnormality in myotonic dystrophy may represent a manifestation of the purported specific cell membrane defect underlying the disease. This is the first report of an abnormality in proopiomelanocortin peptide release in myotonic dystrophy.

Adolescent↗
PubMed1987

Influence of age on neurotransmitter function.

Regulation by neurotransmitters of anterior pituitary hormone secretion is complex and a thorough understanding of their normal role in hormone secretion is a prerequisite to understanding their involvement in age-related changes in endocrine function. To date, uncertainties far out-number demonstrated causative relationships between alterations in neurotransmitter release and resulting age-associated changes in hormone secretion. The best demonstrated relationships are the following. First, a decline in function of the TIDA system is responsible, in part, for the age-related elevation in prolactin secretion and may be involved in the decline in LH secretion. Second, the age-related decrease in hypothalamic norepinephrine turnover plays a role in the decline in LH and GH secretion and may be involved in alterations in TSH secretion during aging. Third, the decline in circadian activity of suprachiasmatic nucleus serotoninergic neurons may account for the blunting of circadian rhythms in the secretions of several anterior pituitary hormones in old animals. Fourth, evidence exists for an age-related decline in function of LHRH neurons, which may contribute to the observation of blunted LH secretion in old animals. Finally, somatostatin release may be increased in old animals, which likely contributes to the age-related decline in GH secretion. Other hypothalamic-releasing hormones have only recently been isolated and characterized; thus, little research on their age-related alterations has been done. Research on these neuropeptides will contribute further to our understanding of the role of neurotransmitters in age-related alterations in hormone secretion.

Aging↗
PubMed1987

[Contribution of immunocytochemistry to the study of the development of neuroglandular peptidergic systems in the human fetal hypothalamus].

Immunohistochemistry makes possible the in situ detection of neuropeptides in the cell bodies were they are synthesized, in the fibers that carry them, and in endings. Immunohistochemistry appears necessary to identify and map peptidergic neurons and to study their ontogeny. From 1975, we have carried the immunohistochemical study of several hypothalamic neuronal populations in the human fetus: LH-RH (1976), somatostatin (1977), pro-opiocortin (1978), vasopressin and oxytocin (1979), corticoliberin (1982), somatocrinin (1983), and hypothalamic neurons containing an unidentified peptide (1984). Comparative ontogenetical studies have also been performed in rats.

Animals↗
PubMed1988

[Monoclonal antibodies to alpha-endorphin effective in immunohistochemistry and immunoblotting].

Four mouse monoclonal antibodies (E11, A8, F8, H5) to alpha-endorphin have been produced. The antibodies bind 12.5, 20.6, 9.6, 6.6% of 125I-beta-endorphin and 35.5, 15.1, 12.8, 12.2% of 125I-gamma-endorphin; the binding of 125I-alpha-endorphin being taken for 100%. The binding of antibodies E11, A8, F8 and H5 to 125I-alpha-endorphin was 50% inhibited by unlabeled ligand in concentrations 5, 50, 30 and 35 nM respectively. Using tissue sections of rat pituitary it was shown that antibody E11 can be used for the localization of endorphin producing cells by immunofluorescence. The antibodies F8 and H5 effectively detected endorphin precursor proopiomelanocortin by immunoblotting.

Animals↗
PubMed1988

Expression and dexamethasone regulation of the human corticotropin-releasing hormone gene in a mouse anterior pituitary cell line.

The factors controlling the expression of corticotropin-releasing hormone (CRH), a hypothalamic neuropeptide involved in the regulation of ACTH secretion, are poorly understood partly because a suitable in vitro model is lacking. To study the regulation of CRH gene expression, an 8-kilobase (kb) DNA fragment containing the entire human CRH gene as well as approximately 6 kb of 5' sequence and 0.8 kb of 3' sequence was isolated from a lambda Charon 4A human genomic library and introduced into a mouse anterior pituitary cell line, AtT-20, by CaPO4 transfection with a neomycin-selectable marker. Approximately 10% of the neomycin-resistant lines stably expressed the CRH gene and secreted radioimmunoassay-detectable CRH into culture media at levels greater than 100 pg/ml. By Southern blot analysis the 8-kb DNA fragment containing the CRH gene had been incorporated intact into the AtT-20 genome. In each CRH-producing strain, but not in the parent AtT-20 cell line, we detected by Northern blot analysis an RNA species that hybridized to two radioactive cRNA probes specific for either the 5' or 3' portion of CRH mRNA, and that co-migrated with placental CRH mRNA. Dexamethasone treatment for 24-96 h caused a specific decrease in CRH mRNA and peptide levels of 40-50% in the five CRH-producing cell lines with half-maximal suppression at approximately 10(-9) M dexamethasone, indicating that CRH gene expression is negatively regulated by glucocorticoids. Thus, we have established an in vitro model suitable for studying in detail those cis- and trans-acting factors which regulate CRH gene expression.

Animals↗
PubMed1985

Endorphins and exercise in females: possible connection with reproductive dysfunction.

Currently available measurements of beta-endorphin and beta-lipotropin in exercising women are in excellent agreement and indicate a 2-3 fold increase over basal levels. Possible effects of exercise upon the transfer of endorphins from the peripheral circulation to the brain are examined, and evidence is presented that suggests the occurrence of a concomitant exercise-related increase of endorphins in both humoral and central nervous system compartments. Steady-state measurements of circulating luteinizing hormone and follicle-stimulating hormone levels in oligo-amenorrheic athletes, on the other hand, do not agree. It is felt that the lack of consensus may be attributable partly to technical inadequacies and partly to lack of awareness of the need for frequent sampling. The bulk of the findings suggest a tendency for luteinizing hormone levels to be low and follicle-stimulating hormone levels to be normal or low, a pattern compatible with repeated activation of the CRH-ACTH-POMC system as a result of exercise.

Adrenocorticotropic Hormone↗
PubMed1985

DNA restriction fragment analysis of the proopiomelanocortin gene in schizophrenia and bipolar disorders.

The method of DNA restriction fragment analysis using gene probes for the proopiomelanocortin (POMC) gene was employed to detect possible molecular variation in the POMC gene in schizophrenia and bipolar illness. No gross structural abnormalities in restriction fragments were observed with the set of restriction enzymes used. Two allelic restriction sites were observed giving rise to fragment length polymorphisms. One of these is a new polymorphism, not previously reported, which will be of value as a linkage marker. The associations between the two DNA polymorphisms that are closely linked to the POMC gene and both schizophrenia and bipolar disorder were investigated. No association was found, thus adding weight to the evidence that there are no alterations in the POMC gene in schizophrenia and bipolar illness.

Base Sequence↗
PubMed1985

[Endogenous opioids].

The discovery of the opioid receptors and their corresponding ligands, the opioid peptides, is of fundamental importance as regards our understanding of a variety of functional mechanisms in the central and peripheral nervous system. This review considers the distribution of the multiple opioid peptides within the organism as well as their tissue-specific enzymatic processing. These parameters differ considerably between species. The multiple opioid peptides are paralleled by multiple opioid receptors. These opioid systems affect a broad spectrum of functions, such as behaviour, pain perception, the cardiovascular system, respiration, appetite, gut motility and secretion, water- and electrolyte balance and the complex field of endocrine mechanisms. The task of future pharmacological research is to study these functions by means of more selective opioid agonists and antagonists. An awareness of our present knowledge and of probable findings to come suggests novel therapeutic possibilities in the field of veterinary science.

Animals↗
PubMed1985

Reflex responses to reductions in functioning renal mass.

Both acute unilateral nephrectomy (AUN) and unilateral ureteral obstruction (UUO) result in an acute increase in cation excretion from the contralateral kidney. AUN results in reflex changes in systemic hemodynamics owing to an acute and transient increase in arterial pressure that activates carotid sinus baroreceptors and constitutes an afferent limb in the reflex; hemodynamic adjustments and increased cation excretion result. The reflex involves participation of the endogenous opioid system, with receptors located primarily in the central nervous system, and requires intact pituitary function because both hypophysectomy and pretreatment with large doses of dexamethasone prevent the postnephrectomy natriuresis. The natriuresis is closely correlated with an increase in the plasma concentration of the NH2-terminal fragment of the pituitary peptide precursor molecule proopiomelanocortin, which suggests that such a peptide could participate directly or indirectly in the postnephrectomy natriuresis. Surgical denervation of either the ipsilateral or the contralateral kidney markedly alters the response to AUN, which prevents the natriuresis and blunts the kaliuresis, and indicates a role for renal neural reflexes. Renorenal reflex pathways also mediate the response of the contralateral kidney to UUO, because denervation of either the ipsilateral (obstructed) or the contralateral kidney abolishes both the natriuresis and kaliuresis usually seen after UUO. This reflex also involves the endogenous opioid system, for it does not occur in rats receiving an i.v. infusion of the opiate receptor antagonist naloxone.

Adaptation, Physiological↗
PubMed1985

Hyperpigmentation, vitiligo, and Addison's disease.

Addison's disease is an uncommon disorder whose dermatologic manifestations range from vitiligo to hyperpigmentation. The association of adrenal autoantibodies and vitiligo has made the latter a possible cutaneous marker for an autoimmune cause. The other cutaneous marker, hyperpigmentation, is now more clearly understood on the basis of a prohormone common to both adrenocorticotrophic hormone (ACTH) and melanocyte-stimulating hormone (MSH).

Addison Disease↗