Hyperendorphinemia in obesity and relationships to affective state

Facchinetti, Fabio; Giovannini, C; Barletta, C; Buzzetti, Raffaella; Burla, Franco; Lazzari, Renato; Genazzani, Ar; Scavo, D

doi:10.1016/0031-9384(86)90456-7

Cited by 34 publications

(20 citation statements)

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“…The increase of B-Ep in obese subjects confirms preliminary data (Givens, Widemann, Andersen and Kitabchi 1980;Facchinetti, Giovannini, Barletta, Petraglia, Buzzetti, Burla, Lazzari, Genazzani and Scavo 1986) suggesting that obesity could be due to a disfunction of the opioid system, although the reason for such increases are unknown. The increase of ACTH plasma level as well as those of B-Ep in 3 cases could be due to the common origin of these peptides from the anterior pituitary cleavage of the same precursor (POMC).…”

Section: Discussionsupporting

confidence: 80%

“…However, the lack of B-Ep circadian rhythm in obese children (Genazzani, Petraglia, Pintor, Giovannini, Severi and Facchinetti 1985) and the increased B-Ep which is desamethasone resistant in obese adults (Facchinetti et al 1986) led to the hypothesis that other sources of POMC derived peptides could contributed to B-Ep disfunction of obese patients.…”

Section: Discussionmentioning

confidence: 96%

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Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

Scavo¹,

Facchinetti²,

Barletta³

et al. 1987

Horm Metab Res

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In order to clarify the possible interaction between endogenous opioids and glucose homeostasis in obesity we studied Beta-Endorphin (B-Ep), ACTH, cortisol and insulin plasma levels in response to an oral glucose tolerance test (OGTT) in 8 females suffering from uncomplicated obesity and in 6 healthy volunteers of normal weight. Results were evaluated in terms of secretion areas subtracted from basal value. Basal glucose, insulin and B-Ep levels were significantly higher in the obese patients compared to controls, cortisol levels and ACTH were not statistically different between obese and normal subjects. During OGTT total areas of insulin secretion were significantly higher in the obese patients; cortisol, ACTH, B-Ep plasma levels did not change in controls, whereas obese patients showed a response to B-Ep which reached a peak at 60 minutes. The area of B-Ep response to OGTT in obese patients was significantly higher than in controls. On the basis of these results we may suggest that the opioid system belongs to the chain of neuroendocrine and metabolic events responsible for the origin and the growth of overweight. But the possibility exists that obesity itself can enhance the B-Ep secretion above all through overeating. In this regard it is to stress that glucose ingestion induces in obese patients, differently from normal subjects, insulin hypersecretion and the B-Ep secretion, possibly from gastro-enteric tract and/or pancreatic isles.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 96%

Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

Scavo¹,

Facchinetti²,

Barletta³

et al. 1987

Horm Metab Res

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“…Introduction P-Endorphin and other endogenous opioid peptides have been shown to be involved in feeding behavior and it has been reported that plasma P-endorphin levels are increased in obese humans [1][2][3][4]. Next to the pituitary as a source of circulating p-endorphin.…”

mentioning

confidence: 99%

β-Endorphin and Insulin/Glucose Responses to Different Meals in Obesity

Zelissen¹,

Koppeschaar²,

Thijssen³

et al. 1991

Horm Res

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The responses of plasma β-endorphin, insulin and glucose to two different isocaloric mixed meals – high carbohydrate (CHO meal) and high fat (fat meal) – were assessed in women with android obesity before (n = 11) as well as after (n = 5) weight reduction, and in normal-weight controls (n = 8). Basal plasma β-endorphin concentrations in the obese subjects (7.7 ± 1.2 pmol/l) were significantly (p < 0.005) higher than in the controls (3.8 ± 0.5 pmol/l) and were not influenced by weight loss. Fasting plasma levels and the integrated releases of insulin and glucose, both after the CHO meal and after the fat meal were significantly higher in the obese subjects than in the controls. The fat meal induced no changes in β-endorphin levels in either group. After the CHO meal a significant decrease in plasma β-endorphin concentration was observed only in the obese group before weight reduction. An influence on β-endorphin release by macronutrients is hypothesized.

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“…The anterior pituitary secretion is inhibited by noradrenaline while the intermediate pitu itary secretion is inhibited by dopamine [Vermes et al, 1980;McLaughlin et al, 1984]. In man, there is no ana tomical evidence of an intermediate pituitary; however, in specific pathophysiological situations the existence of an intermediate-like secretion of p-EP has been sug gested [Wilkers et al, 1980;Lamberts et al, 1982;Facchinetti et al, 1986;Genazzani et al, 1986], It is thus possible that there is a different origin and therefore a different regulation of p-EP and p-LPH also in sub groups of schizophrenics. This could account for the dis sociation in the responses of the two peptides to psycho tropic drugs.…”

Section: Discussionmentioning

confidence: 99%

Effects of Neuroleptic Treatments on Peripheral Opioid Secretion

et al. 1987

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The effects of short- and long-term neuroleptic therapy on peripheral secretion of β-endorphin (β-EP) and β-lipotropin (β-LPH) were examined in 25 chronic schizophrenic patients. Haloperidol was given to 8 patients for 10 days (group A: 0.1 mg/kg b.w./day) and to another group of 8 patients for 30 days (group B: 10–18 mg/day). The other 9 patients were given a combination of haloperidol (6–30 mg/day) with either chlorpromazine (25–75 mg/day), clotiapine (40–60 mg/day), or fluphenazine decanoate (25–75 mg/month) for 14–18 months (group C). β-EP and β-LPH levels were assayed before and after each treatment. Haloperidol plasma levels were assayed in group B patients at the end of treatment. β-EP mean basal levels were higher in patients than in controls; however, β-LPH mean basal levels were higher only for group A patients. After treatment, the mean levels did not differ from those prior to therapy in groups A and B, while β-LPH levels were significantly higher in group C. Level increases or decreases in single patients did not correlate with drug dose or duration of treatment, with baseline peptide levels or with the clinical effects of the various treatments.

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Hyperendorphinemia in obesity and relationships to affective state

Cited by 34 publications

References 20 publications

Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

β-Endorphin and Insulin/Glucose Responses to Different Meals in Obesity

Effects of Neuroleptic Treatments on Peripheral Opioid Secretion

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Hyperendorphinemia in obesity and relationships to affective state

Cited by 34 publications

References 20 publications

Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

Plasma Beta-Endorphin in Response to Oral Glucose Tolerance Test in Obese Patients

&beta;-Endorphin and Insulin/Glucose Responses to Different Meals in Obesity

Effects of Neuroleptic Treatments on Peripheral Opioid Secretion

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β-Endorphin and Insulin/Glucose Responses to Different Meals in Obesity