Twenty-four hour plasma levels of growth hormone and prolactin in Huntington's disease.

Durso, Raymon; Tamminga, Carol A.; Ruggeri, S.; Denaro, A.; Kuo, Shirley; Chase, Thomas N.

doi:10.1136/jnnp.46.12.1134

Cited by 16 publications

(12 citation statements)

References 16 publications

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“…In our study, we found no significant difference in morning, fasting levels of GH or IGF-1, which is in agreement to several previous studies [ 87 – 90 ]. In a 24-hour study of plasma GH concentration in female HD patients free from centrally-active medication and matched controls, Durso et al showed increased levels of GH in HD females throughout the 24-hour period [ 91 ], which is in contrast to our findings. However, it is known in women that the amplitude of GH secretory pulses correlate with circulating levels of oestradiol [ 93 , 94 ].…”

Section: Discussioncontrasting

confidence: 99%

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A 24-Hour Study of the Hypothalamo-Pituitary Axes in Huntington’s Disease

Kalliolia¹,

Silajdžić

Nambron³

et al. 2015

PLoS ONE

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BackgroundHuntington’s disease is an inherited neurodegenerative disorder characterised by motor, cognitive and psychiatric disturbances. Patients exhibit other symptoms including sleep and mood disturbances, muscle atrophy and weight loss which may be linked to hypothalamic pathology and dysfunction of hypothalamo-pituitary axes.MethodsWe studied neuroendocrine profiles of corticotropic, somatotropic and gonadotropic hypothalamo-pituitary axes hormones over a 24-hour period in controlled environment in 15 healthy controls, 14 premanifest and 13 stage II/III Huntington’s disease subjects. We also quantified fasting levels of vasopressin, oestradiol, testosterone, dehydroepiandrosterone sulphate, thyroid stimulating hormone, free triiodothyronine, free total thyroxine, prolactin, adrenaline and noradrenaline. Somatotropic axis hormones, growth hormone releasing hormone, insulin-like growth factor-1 and insulin-like factor binding protein-3 were quantified at 06:00 (fasting), 15:00 and 23:00. A battery of clinical tests, including neurological rating and function scales were performed.Results24-hour concentrations of adrenocorticotropic hormone, cortisol, luteinizing hormone and follicle-stimulating hormone did not differ significantly between the Huntington’s disease group and controls. Daytime growth hormone secretion was similar in control and Huntington’s disease subjects. Stage II/III Huntington’s disease subjects had lower concentration of post-sleep growth hormone pulse and higher insulin-like growth factor-1:growth hormone ratio which did not reach significance. In Huntington’s disease subjects, baseline levels of hypothalamo-pituitary axis hormones measured did not significantly differ from those of healthy controls.ConclusionsThe relatively small subject group means that the study may not detect subtle perturbations in hormone concentrations. A targeted study of the somatotropic axis in larger cohorts may be warranted. However, the lack of significant results despite many variables being tested does imply that the majority of them do not differ substantially between HD and controls.

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Section: Discussioncontrasting

confidence: 99%

“…Studies analysing GH concentration in HD have yielded conflicting results with four studies reporting no significant difference between HD patients and controls [ 87 – 90 ], and three studies reporting an increase in HD [ 24 , 25 , 91 ]. GH exerts its effects by stimulating IGF-1 release from the liver.…”

Section: Discussionmentioning

confidence: 99%

A 24-Hour Study of the Hypothalamo-Pituitary Axes in Huntington’s Disease

Kalliolia¹,

Silajdžić

Nambron³

et al. 2015

PLoS ONE

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“…(1977) and was suggested as being caused by alterations in central dopaminergic neurotransmission. Increased levels of growth hormone have been found after pharmacological stimulation by apomorphine, a dopamine agonist (Durso et al ., 1983). Decreased levels of prolactin have also been reported in HD (Hayden et al ., 1977; Kremer et al ., 1989).…”

Section: Neuropeptidesmentioning

confidence: 99%

“…Decreased levels of prolactin have also been reported in HD (Hayden et al ., 1977; Kremer et al ., 1989). However, other groups have found no alterations in levels of prolactin (Murri et al ., 1980; Lavin et al ., 1981; Durso et al ., 1983) or growth hormone (Murri et al ., 1980; Kremer et al ., 1989). Hence, conflicting results have been found in these reports with regard to prolactin and growth hormone levels in HD and no conclusions can be drawn from them.…”

Section: Neuropeptidesmentioning

confidence: 99%

Hypothalamic–endocrine aspects in Huntington's disease

Petersén

Björkqvist

2006

Eur J of Neuroscience

168

109

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Huntington's disease (HD) is a hereditary and fatal disorder caused by an expanded CAG triplet repeat in the HD gene, resulting in a mutant form of the protein huntingtin. Wild-type and mutant huntingtin are expressed in most tissues of the body but the normal function of huntingtin is not fully known. In HD, the neuropathology is characterized by intranuclear and cytoplasmic inclusions of huntingtin aggregates, and cell death primarily in striatum and cerebral cortex. However, hypothalamic atrophy occurs at early stages of HD with loss of orexin- and somatostatin-containing cell populations. Several symptoms of HD such as sleep disturbances, alterations in circadian rhythm, and weight loss may be due to hypothalamic dysfunction. Endocrine changes including increased cortisol levels, reduced testosterone levels and increased prevalence of diabetes are found in HD patients. In HD mice, alterations in the hypothalamic-pituitary-adrenal axis occurs as well as pancreatic beta-cell and adipocyte dysfunction. Increasing evidence points towards important pathology of the hypothalamus and the endocrine system in HD. As many neuroendocrine factors are secreted into the cerebrospinal fluid, blood and urine, it is possible that their levels may reflect the disease state in the central nervous system. Investigating neuroendocrine changes in HD opens up the possibility of finding biomarkers to evaluate future therapies for HD, as well as of identifying novel targets for therapeutic interventions.

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“…Initial observations of increased levels of growth hormone (GH), which is released upon dopaminergic stimulation from the hypothalamus, supported this theory [23][24][25] . Follow-up studies found increased basal levels or increased release of GH after stimulation by dopaminergic agonists in HD patients [26][27][28][29][30] . Since dopamine stimulation inhibits prolactin release, the notion of increased dopaminergic activity gained further support from reports of reduced prolactin levels, which would be expected if the dopaminergic tone was high in the hypothalamus [31] .…”

Section: Introductionmentioning

confidence: 99%

Huntington’s Disease – New Perspectives Based on Neuroendocrine Changes in Rodent Models

Petersén¹,

Hult²,

Kirik³

2009

Neurodegener Dis

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Huntington’s disease (HD) is a neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene. Although it is characterized by progressive motor impairments, cognitive changes and psychiatric disturbances are major components of the disease. In addition, recent studies have shown that other non-motor symptoms such as alterations in sleep pattern, disruption of the circadian rhythm and increased energy metabolism are common and occur early. Emerging evidence suggests that the latter symptoms are likely results of disturbed functions of the hypothalamus and neuroendocrine circuits, which are known to be central in the regulation of emotion, sleep and metabolism. Whereas clinical data are essential to define key pathological features of HD, animal models that can recapitulate the neurobiological and behavioral features of the disorder are critical tools to elucidate the underlying pathogenic mechanisms. Recent studies employing different HD rodent models have been instrumental in identifying a number of neuroendocrine alterations as well as in highlighting novel potential disease pathways. This review summarizes the current state of knowledge derived from neuroendocrine studies in rodent models of HD in light of clinical relevance and points to future implications for this emerging field.

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Twenty-four hour plasma levels of growth hormone and prolactin in Huntington's disease.

Cited by 16 publications

References 16 publications

A 24-Hour Study of the Hypothalamo-Pituitary Axes in Huntington’s Disease

A 24-Hour Study of the Hypothalamo-Pituitary Axes in Huntington’s Disease

Hypothalamic–endocrine aspects in Huntington's disease

Huntington’s Disease – New Perspectives Based on Neuroendocrine Changes in Rodent Models

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