Corrigendum: Effects of Caragana korshinskii tannin on fermentation, methane emission, community of methanogens, and metabolome of rumen in sheep.

[This corrects the article DOI: 10.3389/fmicb.2024.1334045.].

Effects of Caragana korshinskii tannin on fermentation, methane emission, community of methanogens, and metabolome of rumen in sheep.

The purpose of this research was to investigate the impact of dietary supplementation of Caragana korshinskii tannin (CKT) on rumen fermentation, methane emission, methanogen community and metabolome in rumen of sheep. A total of 15 crossbred sheep of the Dumont breed with similar body conditions, were divided into three groups (n = 5), which were fed with CKT addition at 0, 2 and 4%/kg DM. The study spanned a total of 74 days, with a 14-day period dedicated to adaptation and a subsequent 60-day period for conducting treatments. The results indicated that the levels of ammonia nitrogen (NH3-N) and acetate were reduced (p < 0.05) in rumen sheep fed with 2 and 4% CKT; The crude protein (CP) digestibility of sheep in 2 and 4% CKT groups was decreased(p < 0.05); while the neutral detergent fiber (NDF) digestibility was increased (p < 0.05) in 4% CKT group. Furthermore, the supplementation of CKT resulted in a decrease (p < 0.05) in daily CH4 emissions from sheep by reducing the richness and diversity of ruminal methanogens community, meanwhile decreasing (p < 0.05) concentrations of tyramine that contribute to methane synthesis and increasing (p < 0.05) concentrations of N-methy-L-glutamic acid that do not contribute to CH4 synthesis. However, CH4 production of DMI, OMI, NDFI and metabolic weight did not differ significantly across the various treatments. To sum up, the addition of 4% CKT appeared to be a viable approach for reducing CH4 emissions from sheep without no negative effects. These findings suggest that CKT hold promise in mitigating methane emissions of ruminant. Further investigation is required to evaluate it effectiveness in practical feeding strategies for livestock.

Exercise and Metformin Intervention Prevents Lipotoxicity-Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK/Nrf2/HO-1 Signaling Pathway in db/db Mice.

Objective: Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) commonly coexist and act synergistically to drive adverse clinical outcomes. This study is aimed at investigating the effects of exercise intervention and oral hypoglycaemic drug of metformin (MET) alone or combined on hepatic lipid accumulation. To investigate if oxidative stress and endoplasmic reticulum stress (ERS) are involved in lipotoxicity-induced hepatocyte apoptosis in diabetic mice and whether exercise and/or MET alleviated oxidative stress or ERS-apoptosis by AMPK-Nrf2-HO-1 signaling pathway. Methods: Forty db/db mice with diabetes (random blood glucose ≥ 250 mg/dL) were randomly allocated into four groups: control (CON), exercise training alone (EX), metformin treatment alone (MET), and exercise combined with metformin (EM) groups. Hematoxylin-eosin and oil red O staining were carried out to observe hepatic lipid accumulation. Immunohistochemical and TUNEL methods were used to detect the protein expression of the binding immunoglobulin protein (BiP) and superoxide dismutase-1 (SOD1) and the apoptosis level of hepatocytes. ERS-related gene expression and the AMPK-Nrf2-HO-1 signaling pathway were tested by western blotting. Results: Our data showed that db/db mice exhibited increased liver lipid accumulation, which induced oxidative and ER stress of the PERK-eIF2α-ATF4 pathway, and hepatocyte apoptosis. MET combined with exercise training significantly alleviated hepatic lipid accumulation by suppressing BiP expression, the central regulator of ER homeostasis, and its downstream PERK-eIF2α-ATF4 pathway, as well as upregulated the AMPK-Nrf2-HO-1 signaling pathway. Moreover, the combination of exercise and MET displayed protective effects on hepatocyte apoptosis by downregulating Bax expression and TUNEL-positive staining, restoring the balance of cleaved-caspase-3 and caspase-3, and improving the antioxidant defense system to prevent oxidative damage in db/db mice. Conclusion: Compared to MET or exercise intervention alone, the combined exercise and metformin exhibited significant effect on ameliorating hepatic steatosis, inhibiting oxidative and ER stress-induced hepatocyte apoptosis via improving the capacity of the antioxidant defense system and suppression of the PERK-eIF2α-ATF4 pathway. Furthermore, upregulation of AMPK-Nrf2-HO-1 signaling pathway might be a key crosstalk between MET and exercise, which may have additive effects on alleviating hepatic lipid accumulation.

[Evaluation on degradation of Karst forest community and human disturbance].

Fire, reclamation, herd, and cut led to degradation of Karst forest in Guizhou Province. Five indexes as height, dominance, percentage of asexual individual, biomass, and percentage of shade-tolerant for evaluating community degradation were selected. Degraded communities were divided into six degraded grades (A-F). Community structure and function fluctuated normally in climax (A) under nature force or light human disturbance. While effect of disturbance was preponderated over the range of community fluctuation, climax community degraded evidently, and degraded degree of communities increased gradually. Degraded grades of communities were consistent to succession stages of degraded community. In degraded process, the key factor was decrease of biomass and shade-tolerant species. Degraded communities due to fire, herd, and reclamation were distributed in grades C-F, and degraded community due to cut was in grades B-C. Amount of asexual individual was influenced by disturbance type, and the amount in degraded communities due to fire and cut was more than that due to reclamation and herd. Degraded degree of different disturbed community was in order of cut community < cleared community < herded community < fired community.