Methane emission by Camelids

Methane emissions from ruminant livestock have been intensively studied in order to reduce contribution to the greenhouse effect. Ruminants were found to produce more enteric methane than other mammalian herbivores. As camelids share some features of their digestive anatomy and physiology with ruminants, it has been proposed that they produce similar amounts of methane per unit of body mass. This is of special relevance for countrywide greenhouse gas budgets of countries that harbor large populations of camelids like Australia. However, hardly any quantitative methane emission measurements have been performed in camelids. In order to fill this gap, we carried out respiration chamber measurements with three camelid species (Vicugna pacos, Lama glama, Camelus bactrianus; n = 16 in total), all kept on a diet consisting of food produced from alfalfa only. The camelids produced less methane expressed on the basis of body mass (0.3260.11 L kg21 d21) when compared to literature data on domestic ruminants fed on roughage diets (0.5860.16 L kg21 d21). However, there was no significant difference between the two suborders when methane emission was expressed on the basis of digestible neutral detergent fiber intake (92.7633.9 L kg21 in camelids vs. 86.2612.1 L kg21 in ruminants). This implies that the pathways of methanogenesis forming part of the microbial digestion of fiber in the foregut are similar between the groups, and that the lower methane emission of camelids can be explained by their generally lower relative food intake. Our results suggest that the methane emission of Australia’s feral camels corresponds only to 1 to 2% of the methane amount produced by the countries’ domestic ruminants and that calculations of greenhouse gas budgets of countries with large camelid populations based on equations developed for ruminants are generally overestimating the actual levels

Single-copy nuclear genes resolve the phylogeny of the holometabolous insects

Background: Evolutionary relationships among the 11 extant orders of insects that undergo complete metamorphosis, called Holometabola, remain either unresolved or contentious, but are extremely important as a context for accurate comparative biology of insect model organisms. The most phylogenetically enigmatic holometabolan insects are Strepsiptera or twisted wing parasites, whose evolutionary relationship to any other insect order is unconfirmed. They have been controversially proposed as the closest relatives of the flies, based on rDNA, and a possible homeotic transformation in the common ancestor of both groups that would make the reduced forewings of Strepsiptera homologous to the reduced hindwings of Diptera. Here we present evidence from nucleotide sequences of six single-copy nuclear protein coding genes used to reconstruct phylogenetic relationships and estimate evolutionary divergence times for all holometabolan orders. Results: Our results strongly support Hymenoptera as the earliest branching holometabolan lineage, the monophyly of the extant orders, including the fleas, and traditionally recognized groupings of Neuropteroidea and Mecopterida. Most significantly, we find strong support for a close relationship between Coleoptera (beetles) and Strepsiptera, a previously proposed, but analytically controversial relationship. Exploratory analyses reveal that this relationship cannot be explained by long-branch attraction or other systematic biases. Bayesian divergence times analysis, with reference to specific fossil constraints, places the origin of Holometabola in the Carboniferous (355 Ma), a date significantly older than previous paleontological and morphological phylogenetic reconstructions. The origin and diversification of most extant insect orders began in the Triassic, but flourished in the Jurassic, with multiple adaptive radiations producing the astounding diversity of insect species for which these groups are so well known. Conclusion: These findings provide the most complete evolutionary framework for future comparative studies on holometabolous model organisms and contribute strong evidence for the resolution of the 'Strepsiptera problem', a long-standing and hotly debated issue in insect phylogenetics

Refeeding-Induced Brown Adipose Tissue Glycogen Hyper-Accumulation in Mice Is Mediated by Insulin and Catecholamines

Brown adipose tissue (BAT) generates heat during adaptive thermogenesis through a combination of oxidative metabolism and uncoupling protein 1-mediated electron transport chain uncoupling, using both free-fatty acids and glucose as substrate. Previous rat-based work in 1942 showed that prolonged partial fasting followed by refeeding led to a dramatic, transient increase in glycogen stores in multiple fat depots. In the present study, the protocol was replicated in male CD1 mice, resulting in a 2000-fold increase in interscapular BAT (IBAT) glycogen levels within 4–12 hours (hr) of refeeding, with IBAT glycogen stores reaching levels comparable to fed liver glycogen. Lesser effects occurred in white adipose tissues (WAT). Over the next 36 hr, glycogen levels dissipated and histological analysis revealed an over-accumulation of lipid droplets, suggesting a potential metabolic connection between glycogenolysis and lipid synthesis. 24 hr of total starvation followed by refeeding induced a robust and consistent glycogen over-accumulation similar in magnitude and time course to the prolonged partial fast. Experimentation demonstrated that hyperglycemia was not sufficient to drive glycogen accumulation in IBAT, but that elevated circulating insulin was sufficient. Additionally, pharmacological inhibition of catecholamine production reduced refeeding-induced IBAT glycogen storage, providing evidence of a contribution from the central nervous system. These findings highlight IBAT as a tissue that integrates both canonically-anabolic and catabolic stimulation for the promotion of glycogen storage during recovery from caloric deficit. The preservation of this robust response through many generations of animals not subjected to food deprivation suggests that the over-accumulation phenomenon plays a critical role in IBAT physiology.</p

Refeeding-induced brown adipose tissue glycogen hyper-accumulation in mice is mediated by insulin and catecholamines.

Brown adipose tissue (BAT) generates heat during adaptive thermogenesis through a combination of oxidative metabolism and uncoupling protein 1-mediated electron transport chain uncoupling, using both free-fatty acids and glucose as substrate. Previous rat-based work in 1942 showed that prolonged partial fasting followed by refeeding led to a dramatic, transient increase in glycogen stores in multiple fat depots. In the present study, the protocol was replicated in male CD1 mice, resulting in a 2000-fold increase in interscapular BAT (IBAT) glycogen levels within 4-12 hours (hr) of refeeding, with IBAT glycogen stores reaching levels comparable to fed liver glycogen. Lesser effects occurred in white adipose tissues (WAT). Over the next 36 hr, glycogen levels dissipated and histological analysis revealed an over-accumulation of lipid droplets, suggesting a potential metabolic connection between glycogenolysis and lipid synthesis. 24 hr of total starvation followed by refeeding induced a robust and consistent glycogen over-accumulation similar in magnitude and time course to the prolonged partial fast. Experimentation demonstrated that hyperglycemia was not sufficient to drive glycogen accumulation in IBAT, but that elevated circulating insulin was sufficient. Additionally, pharmacological inhibition of catecholamine production reduced refeeding-induced IBAT glycogen storage, providing evidence of a contribution from the central nervous system. These findings highlight IBAT as a tissue that integrates both canonically-anabolic and catabolic stimulation for the promotion of glycogen storage during recovery from caloric deficit. The preservation of this robust response through many generations of animals not subjected to food deprivation suggests that the over-accumulation phenomenon plays a critical role in IBAT physiology

Dietary Selenium Deficiency Partially Mimics the Metabolic Effects of Arsenic

Chronic arsenic exposure via drinking water is associated with diabetes in human pop-ulations throughout the world. Arsenic is believed to exert its diabetogenic effects via multiple mechanisms, including alterations to insulin secretion and insulin sensitivity. In the past, acute arsenicosis has been thought to be partially treatable with selenium supplementation, though a potential interaction between selenium and arsenic had not been evaluated under longer-term exposure models. The purpose of the present study was to explore whether selenium status may augment arsenic’s effects during chronic arsenic exposure. To test this possibility, mice were exposed to arsenic in their drinking water and provided ad libitum access to either a diet replete with selenium (Control) or deficient in selenium (SelD). Arsenic significantly improved glucose tolerance and decreased insulin secretion and β-cell function in vivo. Dietary selenium deficiency resulted in similar effects on glucose tolerance and insulin secretion, with significant interactions between arsenic and dietary conditions in select insulin-related parameters. The findings of this study highlight the complexity of arsenic’s metabolic effects and suggest that selenium deficiency may interact with arsenic exposure on β-cell-related physiological parameters

Fed-mouse tissue glycogen concentrations.

<p>Group-housed, fed, male, wild-type, CD1 mice were sacrificed at 19∶30, 23∶30, or 07∶30 and tissues were harvested and snap-frozen in liquid nitrogen. Tissue glycogen concentrations were measured in epididymal adipose tissue (EPI) (<b>A</b>), interscapular brown adipose tissue (IBAT) (<b>B</b>), and liver (<b>C</b>). Error bars are ±SEM. Statistical comparisons for each tissue were made between time points using a 2-tailed Student’s t-test. ^#, p<0.001. 10–30 mice were used for each time point.</p

Tissue glycogen during refeeding after total starvation.

<p>Male, wild-type, CD1 mice were starved for either 72 hr (<b>A–C</b>) or 24 hr (<b>D,E</b>) and then sacrificed (0) or allowed to refeed <i>ad libitum</i> 1–48 hr before sacrifice (1–48). Tissues were harvested and snap-frozen in liquid nitrogen. Tissue glycogen was measured in EPI (<b>A</b>), IBAT (<b>B, D</b>), and liver (<b>C, E</b>). Error bars are ±SEM. Statistical comparisons were made between the starved time point (0) and each refeeding time point (1–48) for each tissue using a 2-tailed Student’s t-test. *, p<0.05; **, <i>p<0.01</i>; ^#, <i>p<0.001</i>; ^&, <i>p<0.0001.</i> Fasting time points utilized 3–5 mice, except 24 hr fasting BAT glycogen which utilized 19 mice. All refed measurements were taken from 3–9 mice except 24 hr fasted/refed 2 hr BAT time point, which was measured in 15 mice.</p

Histological visualization of glycogen storage in IBAT (top row) and liver (bottom row) using Periodic Acid Schiff staining.

<p>Male, wild-type, CD1 mice were either fed ad libitum (<b>A</b>, <b>E</b>), fed 60% of their normal daily intake of chow once daily for 5 days and then sacrificed (<b>B</b>, <b>F</b>), or fed 60% of their normal daily intake of chow once daily for 5 days and then allowed to refeed <i>ad libitum</i> 4 hr (<b>C</b>, <b>G</b>) or 48 hr (<b>D</b>, <b>H</b>) before sacrifice. IBAT (<b>A–D</b>) and liver (<b>E–H</b>) were harvested and immediately placed in formalin fixative solution. Fixed samples were mounted in paraffin, sectioned, and stained using Periodic Acid Schiff staining with Hematoxylin and Eosin counter-staining by the University of Chicago Human Tissue Resources Center.</p