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This review describes the major hormonal factors that determine the balance between human skeletal muscle anabolism and catabolism in health and disease, with specific reference to age-related muscle loss (sarcopenia). The molecular mechanisms associated with muscle hypertrophy are described, and the central role of the satellite cell highlighted. The biological dynamics of satellite cells, varying between states of quiescence, proliferation and differentiation are strongly influenced by local endocrine factors. The molecular mechanisms of muscle atrophy are examined focussing on the causes of sarcopenia and associations with systemic medical disorders. In addition, evidence is provided that the mechanisms of atrophy and hypertrophy are unlikely to be simple opposites. Novel endocrine mechanisms underpinning mechano-transduction include IGF-I subtypes that may differentiate between endocrine and mechanical signals; their interaction with classical endocrine factors is an active area of translational research. Recently acquired knowledge on the mechanism of anabolic effects of androgens is also reviewed. The increasingly recognised role of myostatin, a negative regulator of muscle function, is described, as well as its potential as a therapeutic target. Strategies to counter age-related sarcopenia thus represent an exciting field of future investigation.
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Olfaction plays an important role in sexual maturation and behaviour in the animal kingdom. Evidence that it has the same importance in man is far less convincing and frequently dogged by such anecdotes as the role of pheromones in synchronizing menstrual cyclicity in convents and all-girl schools. Sexual immaturity and defective olfaction do however coexist as an inherited disorder in man (Kallmann's syndrome: Kallmann, Schoenfeld & Barrera, 1944; DeMorsier, 1954; White, Rogol, Brown et al. 1983; Hermanussen & Sippell, 1985; Chaussain, Toublanc, Feingold et al. 1988) and for many years the biological basis of these defects remained enigmatic. Recently, the interrelationship between sexual development and absence of olfaction has been clarified in three mammals: mouse, macaque and man.
Mouse and macaque
A neurobiological basis of hypogonadism and anosmia was first suggested by elegant immunohistochemical studies conducted by Schwanzel-Fukuda & Pfaff (1989a). In the mature mouse, nerve cells that produce
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ABSTRACT
An in-situ isolated rat adrenal perfusion technique has been devised to study the opioid control of neurally mediated adrenomedullary catecholamine release. Adrenomedullary catecholamine secretion was induced by electrical stimulation of the cut end of the left descending thoracic sympathetic chain on platinum electrodes. The half-maximal stimulatory potential (ED50) of the system was 8 V, 20 Hz, with 300μs pulse width. Basal release of catecholamine from the adrenal was constant using a perfusion flow rate of 100–300μl/min, but increased significantly with increasing perfusion temperature over the range 36–38 °C. Following repetitive 30-s stimulation of the left thoracic sympathetic chain, and 3-min fraction collections, the total amount of catecholamine released per fraction remained within 80–100% of the maximum release for up to eight consecutive stimuli. The release of catecholamines was completely blocked by hexamethonium (0·1 mmol/l), but recovered to preblockade values within two further stimuli. Using the ED50 and the first three stimuli as control, the effects of morphine (10 nmol/l–1 mmol/l), d-Ala2-MePhe4-Met-enkephalin-(O5)-ol (DAMME; 10 nmol/l–0·1 mmol/l) and naloxone (10 nmol/l– 10 μmol/l) on the response to the next three stimuli were compared. Morphine, DAMME or naloxone did not significantly alter the amount of catecholamine released by this form of stimulation. Therefore in the rat, under the conditions used, there is no evidence for mu (μ) or delta (†) opiate modulation of neurally mediated catecholamine release from the rat adrenal medulla.
J. Endocr. (1986) 111, 7–15
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ABSTRACT
Alterations in levels of adrenal vein and circulating immunoreactive neuropeptide tyrosine Y (NPY), as well as systemic catecholamine concentrations, have been investigated in the dog after endotoxin administration. Eighteen dogs were anaesthetized with α-chloralose and allowed to breathe spontaneously. Severe shock was produced by the administration of a large bolus of Escherichia coli endotoxin followed by a continuous infusion. In two further animals the left lumbar adrenal vein was cannulated and an intermittent choke allowed retrograde sampling of the adrenal effluent. The production of hypodynamic shock was associated with marked increases in systemic catecholamine concentrations but there were no consistent changes in adrenal vein or systemic immunoreactive NPY levels. In contrast, circulating concentrations of immunoreactive NPY were markedly raised above the normal range in five patients with septic shock.
J. Endocr. (1988) 116, 421–426
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ABSTRACT
Dopamine and morphine modulate GH and LH release, probably at a hypothalamic locus. To investigate this in more detail, we studied the influence of these substances on somatostatin and LH-releasing hormone (LHRH) release from rat hypothalamic fragments in vitro. Hypothalamic fragments were incubated in Earle's medium. After 60 min of preincubation, medium from two 20-min incubations was collected and somatostatin and LHRH levels measured by radioimmunoassay. Dopamine (10 nmol/l–0·1 mmol/l) induced a progressive increase (r = 0·41; P <0·01) in basal somatostatin levels. K + (30 mmol/l)-induced somatostatin release was also increased (r = 0·54; P <0·01) by increasing doses of dopamine. Metoclopramide (10 μmol/l) blocked the dopamine (1 μmol/l)-induced increase in somatostatin release. No significant relationship between dopamine and LHRH was found either basally or after K + (30 mmol/l) stimulation. Basal somatostatin was negatively correlated (r = −0·63; P <0·01) with morphine concentrations. No significant correlation was found after K+ (30 mmol/l) depolarization. Basal LHRH release was not influenced by morphine, while K +(30 mmol/l)-induced release was significantly lower than controls only at a concentration of 10 nmol/l. These results suggest that dopamine and morphine act at a hypothalamic level to modulate GH release through alterations in somatostatin secretion. Dopamine and morphine have no consistent effect on hypothalamic LHRH release.
J. Endocr. (1985) 106, 317–322
