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)

Administration of human beta-endorphin (2.5 mg IV bolus) to three subjects with non-insulin-dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes. In contrast to the hyperglycemic response previously observed in normal subjects following beta-endorphin, these diabetics showed a progressive decline in plasma glucose throughout the study period. This disparity may be related to a relatively greater release of insulin and lesser rise in glucagon observed in diabetic subjects than in nondiabetic subjects. These preliminary findings suggest that further studies to elucidate the role of pancreatic beta-endorphin on glucoregulation may be rewarding.
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PMID:Beta-endorphin stimulates the secretion of insulin and glucagon in diabetes mellitus. 631 55

Acid-ethanol extracts of fetal bovine pancrease were examined for the presence of beta-endorphin-like immunoreactivity. Gel-filtration analyses revealed the presence of a major large-molecular-weight beta-endorphin immunoreactive species of approximately 20K delta. This molecular form maintained its size upon resubmission to gel filtration in the presence of 6 M guanidine hydrochloride, separated from the bulk of the glucagon immunoreactivity upon ion-exchange chromatography, showed proportional dilution in the beta-endorphin radioimmunoassay, and interacted in a biospecific manner with Concanavalin-A-Sepharose.
Diabetes 1984 Mar
PMID:Beta-endorphin-like immunoreactivity in extracts of the fetal bovine pancreas. Column chromatographic characterizations of a high-molecular-weight immunoreactive species. 632 Dec 78

A study was carried out on the basal blood level of adrenocorticotropic hormone (ACTH) in 355 patients with diabetes mellitus by a radioimmunologic method. A significant though quantitatively slight elevation of its average value was established versus that of the healthy controls. The changes established reveal a light dependence on sex, age, duration of the disease, type of diabetes, kind of medicamentosus treatment and blood sugar level. No correlation was also established between the hormonal changes and the vasculardegenerative complications with the exception of its insignificantly higher average value in the patients with proliferative retinopathy. The compensation of diabetes leads to normalization of the hormonal level.
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PMID:[Basal blood level of adrenocorticotropic hormone in diabetes mellitus patients]. 632 72

Intracerebroventricular (ICV) instillation of morphine and beta-endorphin causes centrally induced hyperglycemia. Locally active, endogenous opioids in the central nervous system may, therefore, also be involved in the elevation of blood sugar. This possibility was tested by examining the glucoregulatory response to central glucoprivation induced by ICV administration of 2-deoxy-D-glucose (2DG) in dogs. Administration of 2DG resulted in a rise in plasma glucose and immunoreactive glucagon (IRG) of 108 +/- 19 mg/dl and 70 +/- 20 pg/ml, respectively. These changes were attenuated by the simultaneous central infusion of the opiate antagonist naloxone: plasma glucose levels increased by 77 +/- 14 mg/dl and IRG by 43 +/- 3 pg/ml, both significantly different from the effect of 2DG alone (P less than 0.05-0.01). These findings suggest that opiate receptors participate in the counterregulatory response to central glucoprivation. They also provide a mechanism by which endogenous opioid peptides may play a role in the central regulation of glucose homeostasis.
Diabetes 1984 Jul
PMID:Naloxone decreases centrally induced hyperglycemia in dogs. Evidence for an opioid role in glucose homeostasis. 673 43

Neuropeptide Y (NPY), a major brain neurotransmitter, is expressed in neurons of the hypothalamic arcuate nucleus (ARC) that project mainly to the paraventricular nucleus (PVN), an important site of NPY release. NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action. The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release. The ARC-PVN projection appears to be overactive in insulin-deficient diabetic rats, and could contribute to the compensatory hyperphagia and reduced energy expenditure, and pituitary dysfunction found in these animals; overactivity of these NPY neurons may be due to reduction of insulin's normal inhibitory effect. The ARC-PVN projection is also stimulated in rat models of obesity +/- non-insulin diabetes, possibly because the hypothalamus is resistant to inhibition by insulin; in these animals, enhanced activity of ARC NPY neurons could cause hyperphagia, reduced energy expenditure, and obesity, and perhaps contribute to hyperinsulinemia and altered pituitary secretion. Overall, these findings suggest that NPY released in the hypothalamuss, especially from the ARC-PVN projection, plays a key role in the hypothalamic regulation of energy balance and metabolism. NPY is also found in the human hypothalamus. Its roles (if any) in human homeostasis and glucoregulation remain enigmatic, but the animal studies have identified it as a potential target for new drugs to treat obesity and perhaps NIDDM.
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PMID:Neuropeptide Y, the hypothalamus, and diabetes: insights into the central control of metabolism. 747 13

When an endogenous morphine, beta-endorphin was discovered ten years ago, the fact that this morphine is present in the brain and many other tissues suggested to neurobiologists that these peptide opiates play a role which goes beyond that of a simple modulator of the perception of pain. beta-endorphin is a neurohormone which is secreted by the pituitary gland and reaches all tissues present in the body by diffusion. Many laboratories have investigated variations in serum levels of beta-endorphin under widely varying physiological or pathological conditions. Many references to these studies in the literature have thus demonstrated that beta-endorphins play a role in certain behavioural patterns (stress, alcoholism), in obesity, diabetes and psychiatric diseases. In fact, the activity of beta-endorphins would appear to have an interesting role to play and are a promising feature in the treatment of cerebral aging; in this field, beta-endorphins act not only as neuroregulators of other neurotransmitting substances but also, via calcium channels, exert an effect on the walls of cerebral arterioles. In situ, the role of beta-endorphins at the ionic channel level has been studied using the patch-clamp technique. In 1991, E Neher and B Sakmann received the Nobel Medicine and Physiology Prize for this work. beta-endorphin, which may be the "missing link" between the neuron and the wall of the arteriole, must be considered as being a fundamental neurotransmitter in the same way as well-known substances such as noradrenaline, acetylcholine, serotonin, dopamine and the GABAergic system are also neurotransmitters.
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PMID:Physiology of beta-endorphins. A close-up view and a review of the literature. 752 Feb 95

It is well established that the central alpha 2-adrenergic agonist clonidine can enhance growth hormone (GH) secretion in humans. This effect is most likely due to stimulation of hypothalamic growth hormone releasing hormone (GHRH) release. To determine the potency of the new I1-imidazoline receptor agonist moxonidine to release pituitary hormones, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 mg), or placebo orally according to a randomized, double-blind protocol. Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, clonidine, and moxonidine concentrations. The results were compared to those obtained in a standard GHRH stimulation test (1 microgram/kg i.v.). Serum GH levels increased significantly in response to GHRH, clonidine, and moxonidine. However, the increase was less pronounced in response to clonidine and moxonidine as compared to GHRH (mean +/- SEM): after clonidine, GH increased from 0.2 +/- 0.1 to 5.4 +/- 1.5 ng/ml, p < 0.05; moxonidine increased GH levels from 0.1 +/- 0.04 to 4.8 +/- 1.9 ng/ml (p < 0.05); GHRH caused an increase from 0.01 +/- 0.05 to 14.8 +/- 2.5 ng/ml (p < 0.05). No significant change was observed in the concentration of any other pituitary hormone. We conclude that the new I1-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as clonidine.
Exp Clin Endocrinol Diabetes 1995
PMID:Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH. 758 24

The therapeutic efficacy of sustained dopaminergic stimulation in Cushing's disease (CD), was investigated performing a three-month trial with monthly 50-100 mg injections of a bromocriptine depot preparation (Parlodel LAR, Sandoz) in six patients with CD. Dopaminergic treatment did not consistently influence pituitary-adrenal activity, as judged by plasma ACTH, cortisol and urinary free cortisol levels as well as by clinical findings. Interestingly, treatment with bromocriptine was associated with reappearance of menses in the three patients who were amenorrheic. In the five patients submitted to inferior petrosal sinus sampling, a parallelism between ACTH and PRL concentrations could be observed with a PRL rise, ipsilateral to that of ACTH, ensuing in three patients after administration of corticotropin-releasing hormone. In one patient a 55% reduction in the size of the pituitary adenoma was demonstrated by MRI carried out at the end of treatment. Our findings lead to the following conclusions: a) administration of depot injections of bromocriptine to patients with CD appears unable to correct hypercortisolism, although it can induce restoration of menses in amenorrheic patients; b) enhanced PRL concentrations at the pituitary level are probably involved in the amenorrhea often accompanying Cushing's disease.
Exp Clin Endocrinol Diabetes 1995
PMID:Effect of injectable bromocriptine in patients with Cushing's disease. 758 34

The hypothesis that the stimulatory action of free fatty acids (FFA) in the hypothalamic-pituitary-adrenocortical (HPA) axis occurs in part at the adrenal cortex was evaluated. Pathophysiological concentrations of oleic and linoleic acids, but not stearic or caprylic acid, stimulated steroidogenesis from cultured rat adrenocortical cells (concentrations eliciting 50% of maximal responses, approximately 60 and 120 microM, respectively), with a latency of 90 min. Maximal stimulation of steroidogenesis by both acids was < 50% of that produced by adrenocorticotropic hormone (ACTH) and was blocked by cycloheximide. The maximal steroidogenic response to ACTH was inhibited approximately 50% by oleic acid. The actions of oleic and linoleic acids were not associated with an increase in adenosine 3',5'-cyclic monophosphate (cAMP) secretion but appeared to require intracellular oxidation. None of the lipids influenced cell viability or corticosterone radioimmunoassay. The latency of the steroidogenic response, the putative requirement for intracellular oxidation, and the apparent lack of involvement of cAMP suggest a mechanism of action of FFA distinct from that of ACTH, yet still requiring protein synthesis. It is concluded that the modulation of steroidogenesis by these abundant naturally occurring lipids may be an important component of the control mechanisms within the HPA pathway in disorders of lipid homeostasis (e.g., obesity, starvation, or diabetes).
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PMID:Stimulation of steroidogenesis in cultured rat adrenocortical cells by unsaturated fatty acids. 761 25

In order to investigate the relationships between glucose metabolism, insulin secretion and endogenous opioids in obese patients, we have studied the effects of a naloxone infusion on insulin and C-peptide release after a normal meal (800 kcal) eaten at 12.00 hr in 16 obese women, aged 20-61 yr, with a BMI ranging from 25 to 37.2 kg/m2, with normal glucose tolerance (Group 1) and with NIDDM (Group 2). Naloxone was administered in a bolus of 1.6 mg i.v., followed by a continuous infusion of 4 mg in 2 hr starting immediately after feeding. In Group 1 naloxone infusion significantly increased the glucose levels, but insulin secretion was unaffected. In Group 2, naloxone infusion failed to modify significantly the postprandial levels of glucose, insulin and C-peptide. Therefore, in our study naloxone infusion seems to have beta-endorphin-like effects in non-diabetic obese subjects by increasing their glycemic levels, with no evidence of expected insulin decrease. In diabetic obese patients we observed a trend towards decrease in glycemic values during naloxone infusion, as expected, due to insulin plasma levels increase. By these data we can hypothesise a complex regulatory role of opioids in metabolic balance in obesity. In diabetic patients, naloxone can improve the surviving insulin secretion with better glucose tolerance. In non-diabetic subjects naloxone exerts its effects, probably, on peripheral organs.
Diabetes Res 1993
PMID:Naloxone effects on post-prandial glucose, insulin and C-peptide levels in obese subjects. 771 83


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