Global maps of soil temperature

Research in global change ecology relies heavily on global climatic grids derived from estimates of air temperature in open areas at around 2 m above the ground. These climatic grids do not reflect conditions below vegetation canopies and near the ground surface, where critical ecosystem functions occur and most terrestrial species reside. Here, we provide global maps of soil temperature and bioclimatic variables at a 1-km² resolution for 0–5 and 5–15 cm soil depth. These maps were created by calculating the difference (i.e., offset) between in-situ soil temperature measurements, based on time series from over 1200 1-km² pixels (summarized from 8500 unique temperature sensors) across all the world’s major terrestrial biomes, and coarse-grained air temperature estimates from ERA5-Land (an atmospheric reanalysis by the European Centre for Medium-Range Weather Forecasts). We show that mean annual soil temperature differs markedly from the corresponding gridded air temperature, by up to 10°C (mean = 3.0 ± 2.1°C), with substantial variation across biomes and seasons. Over the year, soils in cold and/or dry biomes are substantially warmer (+3.6 ± 2.3°C) than gridded air temperature, whereas soils in warm and humid environments are on average slightly cooler (-0.7 ± 2.3°C). The observed substantial and biome-specific offsets emphasize that the projected impacts of climate and climate change on near-surface biodiversity and ecosystem functioning are inaccurately assessed when air rather than soil temperature is used, especially in cold environments. The global soil-related bioclimatic variables provided here are an important step forward for any application in ecology and related disciplines. Nevertheless, we highlight the need to fill remaining geographic gaps by collecting more in-situ measurements of microclimate conditions to further enhance the spatiotemporal resolution of global soil temperature products for ecological applications

Global maps of soil temperature.

Research in global change ecology relies heavily on global climatic grids derived from estimates of air temperature in open areas at around 2 m above the ground. These climatic grids do not reflect conditions below vegetation canopies and near the ground surface, where critical ecosystem functions occur and most terrestrial species reside. Here, we provide global maps of soil temperature and bioclimatic variables at a 1-km2 resolution for 0-5 and 5-15 cm soil depth. These maps were created by calculating the difference (i.e. offset) between in situ soil temperature measurements, based on time series from over 1200 1-km2 pixels (summarized from 8519 unique temperature sensors) across all the world's major terrestrial biomes, and coarse-grained air temperature estimates from ERA5-Land (an atmospheric reanalysis by the European Centre for Medium-Range Weather Forecasts). We show that mean annual soil temperature differs markedly from the corresponding gridded air temperature, by up to 10°C (mean = 3.0 ± 2.1°C), with substantial variation across biomes and seasons. Over the year, soils in cold and/or dry biomes are substantially warmer (+3.6 ± 2.3°C) than gridded air temperature, whereas soils in warm and humid environments are on average slightly cooler (-0.7 ± 2.3°C). The observed substantial and biome-specific offsets emphasize that the projected impacts of climate and climate change on near-surface biodiversity and ecosystem functioning are inaccurately assessed when air rather than soil temperature is used, especially in cold environments. The global soil-related bioclimatic variables provided here are an important step forward for any application in ecology and related disciplines. Nevertheless, we highlight the need to fill remaining geographic gaps by collecting more in situ measurements of microclimate conditions to further enhance the spatiotemporal resolution of global soil temperature products for ecological applications

Rôle des anses intestinales dans les effets métaboliques du gastric bypass : apport du modèle porcin

Bariatric surgery has been widely used for more than 20 years and has transformed the management of obesity and its metabolic comorbidities (type 2 diabetes, dyslipidemia,hypertension, obstructive apnea syndrome, non-alcoholic steatohepatitis). Its effects are far superior to those of medical treatment. However, the mechanisms of action of bariatric surgery are incompletely understood. The existence of numerous procedures, with various operating principles, does not facilitate their understanding. The study of the mechanisms of action of bariatric surgery has revealed the digestive tract as a key player, involved in the regulation of food intake but also carbohydrate homeostasis. In gastric bypass, the most effective and one of the most performed procedures, the anatomy of the digestive tract is profoundly modified with the creation of two distinct segments where nutrients circulate on one side, digestive secretions on the other, and a third segment where nutrients and digestive secretions meet. By trial and error, the procedure has evolved over time by modulating the length of one or theother of these loops (always at the expense of the others, the intestine being a finite continuum), raising new questions. Many mechanisms of action seem to be involved after gastric bypass (caloric restriction, biliary diversion, increased metabolism of the alimentary limb, ...). In this work, we focused on intestinal absorption. In a porcine model of gastric bypass,we showed that the length of the biliary limb is a key element of weight loss but does not modify glucose absorption or its post prandial response. These appear to be related to the length of the common limb. After gastric bypass, the different intestinal segments seem to be involved in different effects. Understanding how each of these limbs modulates the effects of gastric bypass will allow for a better understanding of the effects of gastric bypass and,eventually, a personalization of the procedure according to the patient's co-morbidities.La chirurgie bariatrique s’est largement répandue depuis plus de 20 ans et a transformé la prise en charge de l’obésité et de ses comorbidités métaboliques (diabète de type 2,dyslipidémie, hypertension, syndrome d’apnée du sommeil, stéatohépatite non alcoolique). Ses effets sont bien supérieurs à ceux du traitement médical. Les mécanismes d’action de la chirurgie bariatrique sont cependant incomplètement compris. L’existence de nombreuses procédures, aux principes de fonctionnement variés, ne facilite pas leur compréhension.L’étude des mécanismes d’action de la chirurgie bariatrique a fait apparaître le tube digestif comme un acteur clé, impliqué dans la régulation de la prise alimentaire mais également l’homéostasie glucidique. Dans le gastric bypass, procédure la plus efficace et l’une des plus réalisées, l’anatomie du tube digestif est profondément remaniée avec la création de deux segments distincts où circulent d’un côté les nutriments, de l’autre côté les sécrétions digestives et un troisième segment où les nutriments et les sécrétions digestives se rencontrent. Par tâtonnement, la procédure a évolué avec le temps en modulant la longueur de l’une ou l’autre de ces anse (toujours aux dépens des autres, l’intestin étant un continuum fini), soulevant de nouvelles questions. De nombreux mécanismes d’action semblent être impliqués après gastric bypass (restriction calorique, diversion biliaire, hypermétabolisme de l’anse alimentaire, …). Dans ce travail, nous nous sommes focalisés sur l’absorption intestinale.Dans un modèle porcin de gastric bypass, nous avons montré que la longueur de l’anse biliaire est un élément clé de la perte de poids mais ne modifie pas l’absorption du glucose ou sa réponse post prandiale. Celles-ci semblent liées à la longueur de l’anse commune. Après gastric bypass, les différentes anses intestinales semblent impliquer dans des effets différents.Comprendre comment chacune de ces anses module les effets du gastric bypass permettra une meilleure connaissance de ceux-ci et, à terme, une personnalisation de la procédure en fonction des comorbidités du patient

Role of intestinal limbs in the metabolic effects of gastric bypass in a porcine model

La chirurgie bariatrique s’est largement répandue depuis plus de 20 ans et a transformé la prise en charge de l’obésité et de ses comorbidités métaboliques (diabète de type 2,dyslipidémie, hypertension, syndrome d’apnée du sommeil, stéatohépatite non alcoolique). Ses effets sont bien supérieurs à ceux du traitement médical. Les mécanismes d’action de la chirurgie bariatrique sont cependant incomplètement compris. L’existence de nombreuses procédures, aux principes de fonctionnement variés, ne facilite pas leur compréhension.L’étude des mécanismes d’action de la chirurgie bariatrique a fait apparaître le tube digestif comme un acteur clé, impliqué dans la régulation de la prise alimentaire mais également l’homéostasie glucidique. Dans le gastric bypass, procédure la plus efficace et l’une des plus réalisées, l’anatomie du tube digestif est profondément remaniée avec la création de deux segments distincts où circulent d’un côté les nutriments, de l’autre côté les sécrétions digestives et un troisième segment où les nutriments et les sécrétions digestives se rencontrent. Par tâtonnement, la procédure a évolué avec le temps en modulant la longueur de l’une ou l’autre de ces anse (toujours aux dépens des autres, l’intestin étant un continuum fini), soulevant de nouvelles questions. De nombreux mécanismes d’action semblent être impliqués après gastric bypass (restriction calorique, diversion biliaire, hypermétabolisme de l’anse alimentaire, …). Dans ce travail, nous nous sommes focalisés sur l’absorption intestinale.Dans un modèle porcin de gastric bypass, nous avons montré que la longueur de l’anse biliaire est un élément clé de la perte de poids mais ne modifie pas l’absorption du glucose ou sa réponse post prandiale. Celles-ci semblent liées à la longueur de l’anse commune. Après gastric bypass, les différentes anses intestinales semblent impliquer dans des effets différents.Comprendre comment chacune de ces anses module les effets du gastric bypass permettra une meilleure connaissance de ceux-ci et, à terme, une personnalisation de la procédure en fonction des comorbidités du patient.Bariatric surgery has been widely used for more than 20 years and has transformed the management of obesity and its metabolic comorbidities (type 2 diabetes, dyslipidemia,hypertension, obstructive apnea syndrome, non-alcoholic steatohepatitis). Its effects are far superior to those of medical treatment. However, the mechanisms of action of bariatric surgery are incompletely understood. The existence of numerous procedures, with various operating principles, does not facilitate their understanding. The study of the mechanisms of action of bariatric surgery has revealed the digestive tract as a key player, involved in the regulation of food intake but also carbohydrate homeostasis. In gastric bypass, the most effective and one of the most performed procedures, the anatomy of the digestive tract is profoundly modified with the creation of two distinct segments where nutrients circulate on one side, digestive secretions on the other, and a third segment where nutrients and digestive secretions meet. By trial and error, the procedure has evolved over time by modulating the length of one or theother of these loops (always at the expense of the others, the intestine being a finite continuum), raising new questions. Many mechanisms of action seem to be involved after gastric bypass (caloric restriction, biliary diversion, increased metabolism of the alimentary limb, ...). In this work, we focused on intestinal absorption. In a porcine model of gastric bypass,we showed that the length of the biliary limb is a key element of weight loss but does not modify glucose absorption or its post prandial response. These appear to be related to the length of the common limb. After gastric bypass, the different intestinal segments seem to be involved in different effects. Understanding how each of these limbs modulates the effects of gastric bypass will allow for a better understanding of the effects of gastric bypass and,eventually, a personalization of the procedure according to the patient's co-morbidities

Macrophage migration inhibitory factor inhibition is deleterious for high-fat diet-induced cardiac dysfunction.

AimsDevelopment of metabolic syndrome is associated with impaired cardiac performance, mitochondrial dysfunction and pro-inflammatory cytokine increase, such as the macrophage migration inhibitory factor MIF. Depending on conditions, MIF may exert both beneficial and deleterious effects on the myocardium. Therefore, we tested whether pharmacological inhibition of MIF prevented or worsened metabolic syndrome-induced myocardial dysfunction.Methods and resultsC57BL/6J mice were fed for ten weeks with 60% fat-enriched diet (HFD) or normal diet (ND). MIF inhibition was obtained by injecting mice twice a week with ISO-1, for three consecutive weeks. Then, triglycerides, cholesterol, fat mass, glucose intolerance, insulin resistance, ex vivo cardiac contractility, animal energetic substrate utilization assessed by indirect calorimetry and mitochondrial respiration and biogenesis were evaluated. HFD led to fat mass increase, dyslipidemia, glucose intolerance and insulin resistance. ISO-1 did not alter these parameters. However, MIF inhibition was responsible for HFD-induced cardiac dysfunction worsening. Mouse capacity to increase oxygen consumption in response to exercise was reduced in HFD compared to ND, and further diminished in ISO-1-treated HFD group. Mitochondrial respiration was reduced in HFD mice, treated or not with ISO-1. Compared to ND, mitochondrial biogenesis signaling was upregulated in the HFD as demonstrated by mitochondrial DNA amount and PGC-1α expression. However, this increase in biogenesis was blocked by ISO-1 treatment.ConclusionMIF inhibition achieved by ISO-1 was responsible for a reduction in HFD-induced mitochondrial biogenesis signaling that could explain majored cardiac dysfunction observed in HFD mice treated with MIF inhibitor

Differential Unfolded Protein Response in skeletal muscle from non-diabetic glucose tolerant or intolerant patients with obesity before and after bariatric surgery

International audienceAIMS:Not all people with obesity become glucose intolerant, suggesting differential activation of cellular pathways. The unfolded protein response (UPR) may contribute to the development of insulin resistance in several organs, but its role in skeletal muscle remains debated. Therefore, we explored the UPR activation in muscle from non-diabetic glucose tolerant or intolerant patients with obesity and the impact of bariatric procedures.METHODS:Muscle biopsies from 22 normoglycemic (NG, blood glucose measured 120 min after an oral glucose tolerance test, G120 < 7.8 mM) and 22 glucose intolerant (GI, G120 between 7.8 and 11.1 mM) patients with obesity were used to measure UPR activation by RTqPCR and western blot. Then, UPR was studied in biopsies from 7 NG and 7 GI patients before and 1 year after bariatric surgery.RESULTS:Binding immunoglobulin protein (BIP) protein was ~ 40% higher in the GI compared to NG subjects. Contrastingly, expression of the UPR-related genes BIP, activating transcription factor 6 (ATF6) and unspliced X-box binding protein 1 (XBP1u) were significantly lower and C/EBP homologous protein (CHOP) tended to decrease (p = 0.08) in GI individuals. While BIP protein positively correlated with fasting blood glucose (r = 0.38, p = 0.01), ATF6 and CHOP were associated with G120 (r = - 0.38 and r = - 0.41, p < 0.05) and the Matsuda index (r = 0.37 and r = 0.38, p < 0.05). Bariatric surgery improved metabolic parameters, associated with higher CHOP expression in GI patients, while ATF6 tended to increase (p = 0.08).CONCLUSIONS:CHOP and ATF6 expression decreased in non-diabetic GI patients with obesity and was modified by bariatric surgery. These genes may contribute to glucose homeostasis in human skeletal muscle