An abnormality in sebaceous function in phenylketonuria.

Burton, J.L.; Goolamali, S.K.; Shuster, Sam

doi:10.1136/bmj.1.5948.19

Cited by 6 publications

(5 citation statements)

References 12 publications

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“…The relative importance of this putative PRL–SG axis to each gender is also unclear. If the primary physiological function of the PRL–SG axis is to increase perinatal sebum production, then it is perhaps surprising that the same mechanism is evidently present in men (Cotterill et al ., ; Burton, Goolamali & Shuster, ; Schulpis et al ., ; Nitkowska et al ., ). A reasonable hypothesis is that the PRL‐SG axis in males somehow only becomes conspicuous when systemic levels of PRL are pathologically high.…”

Section: Prolactin and Dopaminementioning

confidence: 99%

“…Phenylketonuria (PKU) is another hypo‐dopaminergic condition which features both seborrhoea and elevated PRL levels (Table ) (Burton, Goolamali & Shuster, ; Schulpis et al ., ; Denecke et al ., ; van Spronsen, ; Juhász et al ., ). PKU is an autosomal recessive disease caused by inactivating mutations in the gene coding for phenylalanine hydroxylase, the enzyme responsible for tyrosine synthesis.…”

Section: Prolactin and Dopaminementioning

confidence: 99%

“…Consequently, levels of tyrosine and downstream catecholamines, including dopamine, are reduced in those with PKU (van Spronsen, ). As with PD, the seborrhoea of PKU can be ameliorated by L‐DOPA (Burton, Goolamali & Shuster, ). Overall, loss of dopamine‐mediated inhibition of PRL secretion results in increased sebum production in PKU and PD.…”

Section: Prolactin and Dopaminementioning

confidence: 99%

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Neuroendocrinology and neurobiology of sebaceous glands

et al. 2020

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The nervous system communicates with peripheral tissues through nerve fibres and the systemic release of hypothalamic and pituitary neurohormones. Communication between the nervous system and the largest human organ, skin, has traditionally received little attention. In particular, the neuro-regulation of sebaceous glands (SGs), a major skin appendage, is rarely considered. Yet, it is clear that the SG is under stringent pituitary control, and forms a fascinating, clinically relevant peripheral target organ in which to study the neuroendocrine and neural regulation of epithelia. Sebum, the major secretory product of the SG, is composed of a complex mixture of lipids resulting from the holocrine secretion of specialised epithelial cells (sebocytes). It is indicative of a role of the neuroendocrine system in SG function that excess circulating levels of growth hormone, thyroxine or prolactin result in increased sebum production (seborrhoea). Conversely, growth hormone deficiency, hypothyroidism, and adrenal insufficiency result in reduced sebum production and dry skin. Furthermore, the androgen sensitivity of SGs appears to be under neuroendocrine control, as hypophysectomy (removal of the pituitary) renders SGs largely insensitive to stimulation by testosterone, which is crucial for maintaining SG homeostasis. However, several neurohormones, such as adrenocorticotropic hormone and α-melanocyte-stimulating hormone, can stimulate sebum production independently of either the testes or the adrenal glands, further underscoring the importance of neuroendocrine control in SG biology. Moreover, sebocytes synthesise several neurohormones and express their receptors, suggestive of the presence of neuro-autocrine mechanisms of sebocyte modulation. Aside from the neuroendocrine system, it is conceivable that secretion of neuropeptides and neurotransmitters from cutaneous nerve endings may also act on sebocytes or their progenitors, given that the skin is richly innervated. However, to date, the neural controls of SG development and function remain poorly investigated and incompletely understood. Botulinum toxin-mediated or facial paresis-associated reduction of human sebum secretion suggests that cutaneous nerve-derived substances modulate lipid and inflammatory cytokine synthesis by sebocytes, possibly implicating the nervous system in acne pathogenesis. Additionally, evidence suggests that cutaneous denervation in mice alters the expression of key regulators of SG homeostasis. In this review, we examine the current evidence regarding neuroendocrine and neurobiological regulation of human SG function in physiology and pathology. We further call attention to this line of research as an instructive model for probing and therapeutically manipulating the mechanistic links between the nervous system and mammalian skin.

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Section: Prolactin and Dopaminementioning

confidence: 99%

Section: Prolactin and Dopaminementioning

confidence: 99%

Section: Prolactin and Dopaminementioning

confidence: 99%

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Neuroendocrinology and neurobiology of sebaceous glands

et al. 2020

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“…The existence of a specific sebotrophic hormone, suggested by Shuster and Thody (1974) and others, has not been definite proved as yet. Increased sebum ecretion has been attributed to lipotrophic and melanocyte-stimulating (MSH) hormones, particularly to (¡-.MSH, in parkin sonism Shuster and Thody, 1974), in phenylketonuria (Burton et al, 1975), in certain breast diseases (Gollamali and Shuster, 1975) and during chronic chlorpromazine treatment. Shuster et al (1973), who suggest that the seborrhoea of parkinsonism was due to MSH, in particular 0-MSH, have reported the plasma levels to be increased in some, but not in all patients with parkinsonism.…”

Section: Discussionmentioning

confidence: 99%

<i>L</i>-Dopa and the Secretion of Sebum in Parkinsonian Patients

Streifler¹,

Avrami²,

Rabey³

1980

Eur Neurol

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Sebum secretion was studied in 14 parkinsonian patients before and after 3 months of treatment with L-dopa. An abnormality of sebum secretion was shown to exist in parkinsonism. In 7 patients, successfully treated with L-dopa, sebum secretion diminished and its pattern improved. In all patients, in whom L-dopa treatment did not result in noticeable clinical changes, there was no significant modification in sebum secretion. No change was observed in the secretion of sebum of 5 normal control subjects, who were given L-dopa for 1 week.

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“…In patients with biotinidase deficiency, an autosomal recessive condition (McKusick 253260) (Wolf et al 1985), skin rashes, alopecia, seizures, hypotonia, developmental regression and ataxia occur usually after the age of 3 months. Additionally, seborrhoeic or atopic dermatitis (eczema) are common symptoms in untreated phenylketonuria patients (PKU) (McKusick 261600), and Burton et al (1975) have found that there is an abnormality in their sebaceous gland function. We therefore measured biotinidase activity in plasma of PKU children under dietary treatment ......…”

mentioning

confidence: 99%