Sustainable Extensification as an Alternative Model For Reducing GHG Emissions From Agriculture. The Case of an Extensively Managed Organic Farm in Denmark

<div><p>GHG emissions of an extensively managed Danish organic farm were estimated upstream and on-farm. The results were compared to Danish national levels based on land area and output. Overall, the farm emitted 2.12 t CO₂eq ha⁻¹ yr⁻¹. Excluding land use, land use change, and forestry (LULUCF) related emissions, the combined GHG emissions from energy- and agriculture-based activities at the case farm were 47% lower (per unit area) and 12% higher (per unit output), than GHG emissions from Danish agriculture. With current livestock density (0.64 LU ha⁻¹) and crop production area, the case study farm would supply at average 1,466 kcal per inhabitant per day in Denmark, if the farm was scaled up to Danish national level. With a reduction of livestock density to 0.36 LU ha⁻¹ and proportional cropland area expansion for food production <i>(ceteris paribus)</i>, the case study farm could supply around 4,940 kcal person⁻¹ day⁻¹, matching Danish national levels (including Danish net food export surplus of 41.5%). Simultaneously, the case study farm would have a better GHG balance per unit area and unit output in food, compared to the rest of Denmark. Hence, the case study farm system could serve as an alternative model for Danish agriculture under a sustainable extensification scenario with lower GHG emissions, while maintaining sufficient output for human consumption.</p></div

Myocardial Mitochondrial and Contractile Function Are Preserved in Mice Lacking Adiponectin

<div><p>Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart. At 8 weeks of age, heart weight-to-body weight ratios were not different between adiponectin knockout (ADQ^-/-) mice and wildtypes (WT). In isolated working hearts, cardiac output, aortic developed pressure and cardiac power were preserved in ADQ^-/- mice. Rates of fatty acid oxidation, glucose oxidation and glycolysis were unchanged between groups. While myocardial oxygen consumption was slightly reduced (-24%) in ADQ^-/- mice in isolated working hearts, rates of maximal ADP-stimulated mitochondrial oxygen consumption and ATP synthesis in saponin-permeabilized cardiac fibers were preserved in ADQ^-/- mice with glutamate, pyruvate or palmitoyl-carnitine as a substrate. In addition, enzymatic activity of respiratory complexes I and II was unchanged between groups. Phosphorylation of AMP-activated protein kinase and SIRT1 activity were not decreased, expression and acetylation of PGC-1α were unchanged, and mitochondrial content of OXPHOS subunits was not decreased in ADQ^-/- mice. Finally, increasing energy demands due to prolonged subcutaneous infusion of isoproterenol did not differentially affect cardiac contractility or mitochondrial function in ADQ^-/- mice compared to WT. Thus, mitochondrial and contractile function are preserved in hearts of mice lacking adiponectin, suggesting that adiponectin may be expendable in the regulation of mitochondrial energetics and contractile function in the heart under non-pathological conditions.</p></div

Preserved mitochondrial function in ADQ^-/- hearts following isoproterenol treatment.

<p>Mitochondrial O₂ consumption rates (A), ATP synthesis rates (B), and ATP/O ratios (C) in saponin-permeabilized cardiac fibers of ADQ^-/- and WT mice using glutamate as substrate; n = 4. 2-way ANOVA: § effect of isoproterenol.</p

Preserved mitochondrial OXPHOS complex activities in ADQ^-/- hearts.

<p>Enzymatic activity of complex I subunit NDUFB8 (A), complex II subunit 30kDa (B), and complex IV subunit II (C) in isolated mitochondria of ADQ^-/- and WT hearts; n = 5–6. * p<0.05 vs. WT.</p

Preserved contractile function in ADQ^-/- hearts.

<p>Cardiac power (A), aortic developed pressure (B), cardiac output (C), palmitate oxidation (D), glucose oxidation (E), glycolysis (F), MVO₂ (G), and cardiac efficiency (H) in isolated working hearts of ADQ^-/- and WT mice at 8 weeks of age; n = 4–6 for substrate oxidation, n = 10 for contractile parameters. (I) Myocardial triacylglycerol levels in ADQ^-/- and WT mice at 8 weeks of age; n = 4–5. * p<0.05 vs. WT.</p

Similar contractile response of ADQ^-/- hearts to isoproterenol stimulation.

<p>Heart weight-to-tibia length ratios (A), and aortic developed pressure (B), cardiac output (C), cardiac power (D), MVO₂ (E), and cardiac efficiency (F) in isolated working hearts of ADQ^-/- and WT mice subjected to 5 days of continuous subcutaneous isoproterenol infusion; n = 4. 2-way ANOVA: § effect of isoproterenol, * p<0.05 vs. WT saline, # p<0.05 vs. ADQ^-/- saline.</p

Myocardial expression of CTRPs.

<p>(A) Myocardial mRNA expression of CTRP1, 3, 4, 5, 6, 7, 9 and 13 in ADQ^-/- mice at 8 weeks of age, relative to WT expression which was set to 1 (indicated by the dotted line); n = 8. (B) Serum CTRP9 protein levels in ADQ^-/- and WT mice at 8 weeks of age; n = 5. * p<0.05 vs. WT.</p

Preserved OXPHOS protein levels and mitochondrial biogenic signaling in ADQ^-/- hearts.

<p>AMPK phosphorylation (A), SIRT1 activity (B), lysine acetylation (Lys-Ac) of PGC-1α (C), mRNA expression of OXPHOS subunits (D), mRNA expression of mitochondrial biogenesis signaling molecules (E), mRNA expression of fatty acid oxidation genes and PPARα (F), and mitochondrial protein levels of OXPHOS complexes I (NDUFB8 subunit; G), II (Fp subunit; H), and IV (subunit IV; I) in hearts of ADQ^-/- and WT mice at 8 weeks of age; n = 4–5. Myocardial mRNA expression is expressed relative to WT expression which was set to 1 (indicated by the dotted line). * p<0.05 vs. WT.</p

Preserved mitochondrial function in ADQ^-/- hearts.

<p>Mitochondrial O₂ consumption rates, ATP synthesis rates, and ATP/O ratios in saponin-permeabilized cardiac fibers of ADQ^-/- and WT mice, using palmitoyl-carnitine (A-C), glutamate (D-F), or pyruvate (G-I) as substrate; n = 6.</p

A holistic assessment of greenhouse gas dynamics from forests to the effects of wood products use in Austria

<p>Anthropogenic GHG emissions add a fast reinforcing feedback cycle to global carbon dynamics which continues to influence GHG concentrations in the Earth's atmosphere. When looking at forest carbon cycles there is potential in utilizing another feedback cycle, namely the carbon cycle involving harvested wood products. To assess the potential of the mitigation options arising from these carbon flows, the forest-based sector in Austria was modelled to assess causal links, dependencies and dynamics involved in GHG-relevant processes. Carbon dynamics were investigated in forests and forest soil carbon, the forest product chain and life-cycle analyses for substitution of conventional products with wood products in a cascade of different modelling approaches and paradigms, and the results synthesized. It was found that material use of products from domestic timber sources has the highest climate change mitigation efficiency when originating from sustainably managed forests regarding biomass stocks. The emissions saved through building up a carbon stock from harvested wood products and through emissions substitution can be as high as ∼20 years of total annual Austrian emissions in 90 years. Additional conservation measures while sustaining sawnwood production and the related GHG benefits at a high level had the highest contribution to an overall carbon sink.</p