Metabolic scaling in turtles

Bennett and Dawson (1976) presented an analysis of the relationship of metabolic rate (MR) and body mass among turtles, based on 10 studies, but unlike most of other groups of ectotherms, there has been no update to include the many later reports on turtles. Here I present a review of the data on turtle metabolic rates at 20, 25, and 30 °C, along with regression equations and graphical analyses from a large number of studies. Two generalities emerge: (1) reported metabolic rates for sea turtles are higher than for other chelonians, although it is not certain whether this is an intrinsic characteristic of sea turtles or an artifact related to experimental conditions (such as greater activity of sea turtles in metabolic chambers and the fact that a number of studies were done with the turtles out of water), and (2) the slopes of the log–log plots of metabolic rate (MR) vs. body mass [b in the allometric equation MR = a(mass)^b] are mostly lower than previously reported in smaller studies.     

Metabolic scaling of antibiotics in reptiles: Basis and limitations

The allometric equation y = a · x^b has been used to scale many morphological and physiological attributes relative to body mass. For instance, in eutherian mammals, the equation P_met = 70M_b^0.75 has been used to describe the relationship between metabolic rate (P_met) and body mass (M_b). Similar equations have been derived for squamate reptiles. Recently, this relationship between metabolic rate and body mass has been used in determining appropriate dosages and dosing intervals of antibiotics both intraspecifically for different sized reptiles and interspecifically for those reptiles in which antibiotic pharmacokinetic studies have not been performed. Although this is a simple mathematical process, a number of problems surface when this approach is examined closely. First, the mass constant (a) in reptiles varies from 1–5 for snakes and 6–10 for lizards. No such information is available for chelonians or crocodilians. Unless the mass constant for the unknown species approximates that of the known species, inappropriate dosages and intervals of administration will be calculated. Second, pharmacokinetic differences may exist between widely divergent species, independent of metabolic rate. Third, all available pharmacokinetic studies and metabolic allometric equations are derived from clinically healthy reptiles. Differences more than likely exist between healthy and ill reptiles in regard to uptake, distribution, and elimination of drugs and overall metabolism. While metabolic scaling of antibiotics is a potentially useful and practical tool in drug dosing, these limitations must be considered when dosing an ill reptile. Until more scientifically derived information is available for demonstrating the accuracy of metabolic scaling of antibiotics in reptiles, the clinician will need to understand the limitations of this approach. © 1996 Wiley-Liss, Inc.     

Metabolic scaling in insects supports the predictions of the WBE model

The functional association between body size and metabolic rate (BS-MR) is one of the most intriguing issues in ecological physiology. An average scaling exponent of 3/4 is broadly observed across animal and plant taxa. The numerical value of 3/4 is theoretically predicted under the optimized version of West, Brown, and Enquist's vascular resource supply network model. Insects, however, have recently been proposed to express a numerically different scaling exponent and thus application of the WBE network model to insects has been rejected. Here, we re-analyze whether such variation is indeed supported by a global deviation across all insect taxa at the order and family levels to assess if specific taxa influence insect metabolic scaling. We show that a previous reported deviation is largely due to the effect of a single insect family (Termitidae). We conclude that the BS-MR relationship in insects broadly supports the core predictions of the WBE model. We suggest that the deviation observed within the termites warrants further investigation and may be due to either difficulty in accurately measuring termite metabolism and/or particularities of their life history. Future work on allometric scaling should assess the nature of variation around the central tendencies in scaling exponents in order to test if this variation is consistent with core assumptions and predictions of the WBE model that stem by relaxing its secondary optimizing assumptions that lead to the 3/4 exponent.     

Too much of a good thing

Culture of primary lymphocytes at physiological oxygen levels better maintains intracellular redox state.     

Metabolic cost of motility in planktonic protists: Theoretical considerations on size scaling and swimming speed

The metabolic cost of swimming for planktonic protists is calculated, on theoretical grounds, from a simple model based upon Stokes' law. Energetic expenditure is scaled over both typically encountered size ranges (1–100 µm) and swimming speeds (100–5,000 µm/sec). In agreement with previous estimates for typical flagellates, these estimates generally suggest a low (<1%) cost for motility, related to total metabolic rate of growing cells. However, the cost of motility in small, fast-moving forms, such as some ciliates and flagellates, may be significant (1–10%) and even substantial (10–100%+) for certain species. In accordance with these predictions, many fast-moving ciliates restrict motility to bursts of activity or jumps. In the absence of a reduction in swimming speed or in the frequency of jumps, it is predicted that this relative cost of motility will be significantly increased in starving heterotrophs or light-limited autotrophs, if such cells reduce cell volumes and specific rates of respiration.     

Metabolic scaling theory in plant biology and the three oxygen paradoxa of aerobic life

Alfred Russell Wallace was a field naturalist with a strong interest in general physiology. In this vein, he wrote that oxygen (O₂), produced by green plants, is “the food of protoplasm, without which it cannot continue to live”. Here we summarize current models relating body size to respiration rates (in the context of the metabolic scaling theory) and show that oxygen-uptake activities, measured at 21 vol.% O₂, correlate closely with growth patterns at the level of specific organs within the same plant. Thus, whole plant respiration can change ontogenetically, corresponding to alterations in the volume fractions of different tissues. Then, we describe the evolution of cyanobacterial photosynthesis during the Paleoarchean, which changed the world forever. By slowly converting what was once a reducing atmosphere to an oxidizing one, microbes capable of O₂-producing photosynthesis modified the chemical nature and distribution of the element iron (Fe), slowly drove some of the most ancient prokaryotes to extinction, created the ozone (O₃) layer that subsequently shielded the first terrestrial plants and animals from harmful UV radiation, but also made it possible for Earth’s forest to burn, sometimes with catastrophic consequences. Yet another paradox is that the most abundant protein (i.e., the enzyme Rubisco, Ribulose-1,5-biphosphate carboxylase/oxygenase) has a greater affinity for oxygen than for carbon dioxide (CO₂), even though its function is to bind with the latter rather than the former. We evaluate this second “oxygen paradox” within the context of photorespiratory carbon loss and crop yield reduction in C3 vs. C4 plants (rye vs. maize). Finally, we analyze the occurrence of reactive oxygen species (ROS) as destructive by-products of cellular metabolism, and discuss the three “O₂-paradoxa” with reference to A. R. Wallace’s speculations on “design in nature”.     

Metabolic syndrome: a brain disease

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%-50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.     

Methamphetamine induces chronic corticostriatal depression: too much of a bad thing

Leading theories of drug addiction propose that repeated drug exposure produces a long-lasting homeostatic dysregulation in brain reward processing that is normalized by drug readministration. In this issue of Neuron, Bamford and colleagues describe a novel neurobiological substrate that may contribute to this effect.