Plasma β-Endorphin and β-Lipotropin in Patients with Parkinsonʼs Disease

Franceschi, M.; Cecchetto, Roberta; Panerai, Alberto E.; Truci, Giulio; Smirne, Salvatore; Canal, N.

doi:10.1097/00002826-198612000-00006

Cited by 6 publications

(4 citation statements)

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“…It has been suggested that B-lipotrophin and alipotrophin, peptides derived from a common precursor proopiomelanocortin (20), have sebotropic properties. In addition, both of them are under the inhibitory control of the dopaminergic system in brain (21). These data support the idea that both treatments, L-dopa or bromocriptine, decrease sebum secretion by their central dopaminergic actions, in the same way as they improve parkinsonian signs (1 8).…”

Section: Discussionsupporting

confidence: 62%

Sebum secretion in idiopathic Parkinson's disease: effect of anticholinergic and dopaminergic drugs

Villares

Carlini

1989

Acta Neurologica Scandinavica

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Sebum secretion was measured on the foreheads of 47 unmedicated patients with idiopathic Parkinson's disease, aged 50-81 years and 80 healthy, matched volunteers. Sebum secretion was significantly higher in men patients aged 50-59 years than in controls; no such difference was observed in women of the same age. There was also no difference between patients and volunteers of either gender older than 60 years of age. The effects of either biperiden, L-Dopa + benserazide (a decarboxylase inhibitor) or bromocriptine treatments on sebum secretion and on 5 parkinsonian signs were evaluated over 127 days. There was a significant reduction of all measures during the treatment with the dopaminergic drugs. The only observable effect with biperiden was reduction of tremor. It is discussed whether the sebum suppressive effect of the dopaminergic drugs may be explained through their central effects.

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Section: Discussionsupporting

confidence: 62%

Sebum secretion in idiopathic Parkinson's disease: effect of anticholinergic and dopaminergic drugs

Villares

Carlini

1989

Acta Neurologica Scandinavica

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“…In a previous study [5] of untreated PD patients, we found significantly higher plasma beta-endorphin levels than those of control and treated patients. This effect may be due to a reversible TIDA deficit having disinhibited pituitary secretion of beta-endorphin.…”

Section: Discussionsupporting

confidence: 40%

Tuberoinfundibular Dopaminergic Function in Parkinson’s Disease

Franceschi

Camerlingo²,

Perego

et al. 1988

Eur Neurol

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A deficit of nigrostriatal, mesocortical and mesolimbic dopamine systems in Parkinson’s disease is well known. We know less about the involvement of tuberoinfundibular dopamine (TID) systems. In untreated (naive or wash-out) men with Parkinson’s disease, we studied TID function through basal and stimulated plasma levels of growth hormone, prolactin and thyrotropin. Only minor abnormalities in prolactin responses to thyrotropin-releas-ing hormone were found, probably reflecting denervation hypersensitivity. TID function is preserved in men with Parkinson’s disease.

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“…In contrast, POMC has been relatively unexplored (Halabe Bucay, 2008). Indeed, the fate of b-endorphin in PD and dyskinesia is unclear, as one study found higher plasma levels of b-endorphin in PD patients treated with L-DOPA or not (Franceschi et al, 1986), whereas another study found unchanged plasma levels and reduced CSF levels of b-endorphin (Nappi et al, 1985). Neither of these two studies established correlations with dyskinesia.…”

Section: A Preproenkephalin and Preprodynorphinmentioning

confidence: 99%