“You have to eat something”. Everybody knows this sentence from his/her mother/grandmother. And it is actually true. Starvation is life-threatening. So no wonder that the human body takes this matter quite serious and responds with some emergency plans for energy conservation, like e.g. reduction of metabolism and body temperature. But starvation induced reduction in body temperature can not only be found in humans and other mammals but also in ectotherms, such as mosquitoes, cockroaches, and rainbow trout. What about Drosophila (fruit flies)? Yujiro Umezaki, et al. tested if Drosophila also shows starvation-induced body temperature reduction and if so, how they control it. Drosophila are so small, that their body temperature is mainly regulated by the ambient temperature. The small flies actively move to temperature regimes which suits their needs. Yujiro Umezaki, et al. showed, that starvation results in a lower preferred temperature in Drosophila. This process is like other starvation-induced behaviors controlled by the insulin/insulin-like growth factor (IGF) signaling pathway. (It is the same pathway we had in the last paper of the day, for the longevity and egg quality in C.elegans). To make a long story short: Starvation in Drosophila results in an increased expression of insulin-like peptide 6 (Ilp6) in the fat body (fly liver and adipose tissues). Ilp6 then alternates the “warm sensing” (TrpA1) channels of the temperature controlling neurons (anterior cells), so that the “too warm” threshold is decreased. Therefore, the preferred temperature is lower. What is most interesting, and the taking-home message for today is that the IGF signaling pathway is well conserved in vertebrates and invertebrates. It has been shown that starvation-induced decrease in body temperature in mice is controlled by IGF receptors, and Drosophila Ilp6 is functionally and structurally similar to IGFs. Therefore, it seems like the mechanism underlying the starvation-induced reduction in body temperature may be evolutionarily conserved between different species. So your body response to starving is not so different from the body response in Drosophila.
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Your cells know two “dying” programs: apoptosis and necrosis. The latter results in swelling, ripping of the cell membrane, release of the cell content to the environment and therefore inflammation of the neighbour cells. In contrast, apoptosis is the self-induced and well-controlled suicide program of the cell which results in shrinking and fragmentation and doesn’t harm the neighbour cells. However, as always in life, the is not just black and white. Both processes have some similarities, especially in the beginning. Moreover, both can be triggered by similar toxic stimuli, and the “magnitude of the initial insult, rather than the type of the stimulus […] plays a critical role in the decision of the cell to undergo either apoptosis or necrosis.” The “decision” seems to be controlled by the intracellular ATP (energy) concentration, as apopotosis needs much more energy than necrosis. The hypothesis about the interplay between insult magnitude and intracellular ATP was tested by L. Formigli et al. (2000). They treted rat fibroblasts with different concentrations of Antimycin A, a toxin which blocks the mitochondrial respiratory chain and therefore leads to hypoxia (reduced oxygen content) and so to reduced ATP production. Indeed they were abel to show, that low Antimycin A concentrations, which result just in a small damage of the intracellular ATP storages, lead more to apoptosis, while high concentrations, which attack the ATP storages, lead to necrosis. Concentrations between resulted in mixed cell deaths: They showed apoptotic DNA fragmentation and degradation combined with necrotic cytoplasmatic swelling and membrane disruption. This mixed dying strategy L. Formigli et al. named “aponecrosis”. It seems like that cells which experience a toxic stimulus first try apoptosis, when there is still a certain amount of ATP left. However, if the ATP concentrations are depleted before the apoptosis process is finished, the cell switches to necrosis. So message of the day: (I) dying needs energy and (II) there are more than two ways to die. "Aponecrosis: morphological and biochemical exploration of a syncretic process of cell death sharing apoptosis and necrosis."
L. Formigli, et al. Journal of cellular physiology 182.1 (2000): 41-49. The todays paper of the day is about stuttering. When I googled stuttering I found a funny quote: “Stuttering is Ok. Because what I say is worth repeating”. This quote highlights already the most prominent feature of stuttering: the involuntary repetitions of sounds and words which disturb the fluency of speech. Moreover, involuntary prolongations of sounds and involuntary silent pauses in which the person is unable to say anything, are also characteristics of stuttering. Sometimes people stutter in uncomfortable stressful situations, sometimes the stuttering is a persistant disease (also called chronic perseverative stuttering - CPS). The latter is the focus of the paper of Jolanta Góral-Półrola et al. (2015). The neurodevelopmental hypothesis of fluency of speech “suggests that the main symptoms in stuttering disorders are the result of integrated genetic, developmental, neurological, and social factors.” Based on this hypothesis, Góral-Półrola et al. (2015) looked at the gene expression of a 26 years old CPS patient. The focus was on stress related genes. Interestingly, “the expression of almost all tested genes, with the exception of IL1, in patient’s leukocytes were lower than in the control group.” This either means a lower stress load of this patient or insufficient stress response and protection of the cells. Of course, a single patient is not enough for significant study results, but having in mind that the most of us were already in a stressfull situation in which they started stutering, it seems quite logical that chronic stuttering may be connected to an decreased stress tolerance due to low stress gene expression. Just as remark: "Changes in gene expression associated with cell stress in the patient with chronic persevarative stuttering"
Góral-Półrola et al. (2015). |
IdeaI love to increase my general science knowledge by reading papers from different fields of science. Here I share some of them. Archiv
März 2018
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