The tammar wallaby: a non-traditional animal model to study growth axis maturation

2019 ◽  
Vol 31 (7) ◽  
pp. 1276
Author(s):  
Jennifer A. Hetz ◽  
Brandon R. Menzies ◽  
Geoffrey Shaw ◽  
Marilyn B. Renfree

Maturation of the growth hormone (GH)/insulin-like growth factor 1 (IGF1) axis is a critical developmental event that becomes functional over the peripartum period in precocial eutherian mammals such as sheep. In mice and marsupials that give birth to altricial young, the GH/IGF1 axis matures well after birth, suggesting that functional maturation is associated with developmental stage, not parturition. Recent foster-forward studies in one marsupial, the tammar wallaby (Macropus eugenii), have corroborated this hypothesis. ‘Fostering’ tammar young not only markedly accelerates their development and growth rates, but also affects the timing of maturation of the growth axis compared with normal growing young, providing a novel non-traditional animal model for nutritional manipulation. This review discusses how nutrition affects the maturation of the growth axis in marsupials compared with traditional eutherian animal models.

1994 ◽  
Vol 266 (5) ◽  
pp. E776-E785 ◽  
Author(s):  
P. A. Weller ◽  
M. J. Dauncey ◽  
P. C. Bates ◽  
J. M. Brameld ◽  
P. J. Buttery ◽  
...  

Regulation of insulin-like growth factor I (IGF-I) and growth hormone (GH) receptor mRNA in liver and muscle by energy status was assessed in 2-mo-old pigs by altering thermoregulatory demand and energy intake over a 5-wk period to produce a range of plasma IGF-I concentrations from 3.5 +/- 0.7 to 28.9 +/- 6.2 nmol/l. These values were related directly to growth rates (0.06 +/- 0.02 to 0.44 +/- 0.01 kg/day) and total hepatic IGF-I mRNA levels. Increased growth rates were accompanied by an increase in hepatic class 1 and class 2 IGF-I mRNA levels and an increase in the ratio of class 2 to class 1 IGF-I mRNA in liver, suggesting a distinct role for class 2 expression in the endocrine growth response. High levels of class 1 transcripts and a virtual absence of class 2 transcripts characterized all muscle tissues examined, and there was no correlation with plasma IGF-I levels. This suggests that growth promotion in response to increased energy status is regulated via endocrine hepatic IGF-I rather than via a paracrine response. The levels of GH receptor mRNA were positively correlated with overall growth rate (P < 0.005) in liver and negatively correlated (P < 0.05) in muscle, indicating distinct tissue-specific effects of energy status.


1990 ◽  
Vol 2 (1) ◽  
pp. 79 ◽  
Author(s):  
TP Fletcher ◽  
G Shaw ◽  
MB Renfree

Female tammar wallabies were treated with the dopamine agonist bromocriptine at the end of pregnancy to suppress the peripartum pulse of plasma prolactin. The animals were subsequently observed, and a series of blood samples taken to define the hormonal profiles before and immediately after parturition. Birth was observed in 4/5 control animals and occurred in 8/9 bromocriptine-treated animals. The peripartum peak in plasma PGFM concentrations was not affected by bromocriptine although the pulse of prolactin normally seen at parturition was completely abolished. The timing of luteolysis was apparently unaffected, as plasma progesterone concentrations fell similarly in both treated and control animals immediately after parturition. However, all of the neonates of the bromocriptine-treated animals died within 24 h, possibly because of a failure to establish lactation. Subsequent onset of post-partum oestrus was delayed or absent both in control and in bromocriptine-treated animals, suggesting that the frequent blood sampling and disturbances in the peripartum period interfered with these endocrine processes. It is concluded that both prolactin and prostaglandin can induce luteolysis in the pregnant wallaby, but that the normal sequence of events results from a signal of fetal origin inducing a prostaglandin release from the uterus, which in turn releases a pulse of prolactin that induces a progesterone decline.


2009 ◽  
Vol 21 (9) ◽  
pp. 92
Author(s):  
J. C. Fenelon ◽  
G. Shaw ◽  
M. B. Renfree

Embryonic diapause, a suspension of cell division and growth at the blastocyst stage, is widespread amongst mammals, but is especially common in the kangaroos and wallabies. In the tammar, Macropus eugenii, the sequence of endocrine events leading to embryonic diapause and reactivation are well defined[1]. The blastocyst can remain in diapause for up to 11 months without cell division, measurable metabolism or apoptosis occurring [2]. The ovarian hormones, especially progesterone, exert their effects on the blastocyst by alterations in the endometrial secretions [3], but the molecular cross-talk between the endometrium and blastocyst is unknown. There is increasing evidence for the involvement of leukaemia inhibitory factor (LIF)but the epidermal growth factor (EGF) family of growth factors are also likely to be involved.This study examined the expression of EGF and HB-EGF as well as their receptors, ERBB1 and ERBB4, in the tammar endometrium and blastocyst at entry into, and reactivation from, diapause. The genes for these factors were highly conserved in the tammar with orthologues in human and mouse. Quantitative RT-PCR of all four factors in the endometrium showed that expression changed with stage. Although expression levels of both receptors did not change between diapause and reactivation, both HB-EGF and EGF levels increased at reactivation from diapause and levels of HB-EGF decreased at entry into diapause. All factors were immunopositive in the endometrium. Studies underway will determine whether the cellular location and quantity of these factors change with entry into or exit from diapause, and define the molecular interactions occurring between the blastocyst and endometrium. These results are consistent with a role for the EGF family of growth factors in the control of embryonic diapause in tammars.


1994 ◽  
Vol 6 (4) ◽  
pp. 437 ◽  
Author(s):  
RC Jones ◽  
J Clulow

This review compares sperm production in the tammar wallaby and eutherian mammals, particularly the rat. The capacity of sperm to fertilize an ovum when they leave the testis and the changes they undergo in the epididymidis are considered. The structural differentiation and regulation of the extratesticular duct system is assessed and related to the reabsorption and secretion of water, inorganic ions and proteins, and the interaction of sperm and proteins synthesized and secreted by the epididymidis. Adaptations of the cauda epididymidis for storing spermatozoa are also considered. It is suggested that the tammar may be a good animal model to study the suppression of sperm motility and metabolism in the cauda epididymidis as it is possible to collect from them luminal samples of sperm which are initially immotile and then spontaneously activate during incubation in vitro.


2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.


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