Necrophagous flies that colonize human and animal corpses are extremely efficient at locating and utilizing carrion. Adult flies deposit eggs or larvae on the ephemeral food resource, which signals the beginning of intense inter- and intra-species competition. Within a short period of time after egg hatch, large larval aggregations or maggot masses form. A period of intense larval feeding ensues that will culminate with consumption/decomposition of all soft tissues associated with the corpse. Perhaps the most distinctive feature of these feeding aggregations is heat production; that is, the capacity to generate internal heat that can exceed ambient temperatures by 30°C or more. While observations of maggot mass formation and heat generation have been described in the research literature for more than 50 years, our understanding of maggot masses, particularly the physiological ecology of the aggregations as a whole, is rudimentary. In this review, an examination of what is known about the formation of maggot masses is presented, as well as arguments for the physiological benefits and limitations of developing in feeding aggregations that, at times, can represent regions of intense competition, overcrowded conditions, or a microclimate with elevated temperatures approaching or exceeding proteotoxic stress levels.
Development of two species of necrophagous flies, Sarcophaga bullata Parker (Sarcophagidae) and Protophormia terraenovae (Robineau-Desvoidy) (Calliphoridae), was examined in different size maggot masses generated under laboratory conditions. Larvae from both species induced elevated mass temperatures dependent on the number of individuals per mass. The relationship was more evident for S. bullata, as larvae generated higher temperatures in every size maggot mass than P. terraenovae. Several development events were altered with increasing maggot mass size of flesh flies, and to a lesser extent blow flies, which corresponded with elevated temperatures. Duration of development of all feeding larval stages decreased with increased size of maggot mass. However, the length of development during puparial stages actually increased for these same flies. Puparial weights also declined with maggot mass size, as did the ability to eclose. The altered fly development was attributed to the induction of heat stress conditions, which was evident by the expression of heat shock proteins (23, 60, 70, and 90) in larval brains of both fly types.
It is well known that maternal smoking during pregnancy can lead to low birth weight and low body fat in human newborns. The purpose of this study was to determine whether chronic maternal nicotine treatment alters levels of known regulators of energy balance in the newborn offspring. Pregnant rhesus monkeys were treated with nicotine tartrate (1.5 mg/kg x d) starting on d 26 of pregnancy and maintained through d 160 of gestation. Nicotine exposure had no significant effect on absolute birth weights of the neonatal monkeys, although there was a 10% reduction in birth weights with nicotine exposure when they were normalized to maternal weight. Postnatal d 1 plasma leptin levels were significantly reduced by about 50% in the nicotine treatment group compared with saline controls, suggesting that the infant monkeys exposed to nicotine may also have lower body fat levels. In situ hybridization studies demonstrated that chronic nicotine exposure resulted in a significant decrease in arcuate NPY mRNA expression in the neonatal monkeys. In addition, there was a 2-fold increase in POMC mRNA in the arcuate nucleus in the nicotine-exposed group. These data suggest that nicotine exposure during pregnancy may increase energy expenditure in the developing fetus through actions on hypothalamic systems, resulting in lower birth weights and body fat levels.
During lactation, hypothalamic levels of neuropeptide Y (NPY) and agouti related protein (AGRP) mRNA are increased, while pro-opiomelanocortin (POMC) mRNA is decreased. Serum leptin levels are also decreased during lactation. These changes may underlie the large increases of both food and water intake that occur in concert with milk production. However, additional hypothalamic substances, such as the novel peptide, orexin, may be involved. In addition, in the presence of chronically suppressed levels of serum leptin, there may be a change in leptin receptor expression in the hypothalamus. The objectives of the present study were to determine if orexin and leptin receptor mRNA levels were changed during lactation. Rats were studied on dioestrus of the oestrous cycle or on day 10 postpartum (the lactating animals were suckling eight pups). Orexin mRNA levels in the lateral hypothalamus did not differ between dioestrus and lactation. There was a significant increase in leptin receptor mRNA levels in the supraoptic nucleus during lactation compared to dioestrus. Furthermore, leptin receptor protein, as determined by immunocytochemistry, was colocalized in virtually all vasopressin and oxytocin cells in the supraoptic nucleus. Lactating animals exhibited a decrease in leptin receptor mRNA in the ventromedial hypothalamic nucleus whereas no change was apparent in other hypothalamic areas compared to the dioestrus animals. These results demonstrate that changes in orexin do not appear to contribute to the increase in food intake during lactation. It is likely that the increases in NPY and ARGP, coupled with the decrease in POMC, are primarily responsible for sustaining the chronic hyperphagia of lactation. The changes observed in leptin receptor expression in the hypothalamus, along with the suppression of serum leptin levels, also suggest that the leptin signalling system may play a significant role in the regulation of food and water intake during lactation.
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