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Introduction -- Chapter 1. Megatrends affecting agribusiness: from challenges to opportunities -- Chapter 2. Innovation trends in the agribusiness supply chain -- Chapter 3. Agriculture as an asset class in the alternative investments space -- Conclusions.

AbstractOfftaking agreements are an important risk transfer mechanism in project finance. However, they can also be thought of as a trade‐off between lower market and higher counterparty risks. We use the case of the Quezon Power Ltd Co. to test the effect of higher counterparty risk on the cost of funding. Results indicate that the spread of Quezon's bond and counterparty risk are positively correlated when risk is represented by the daily volatility of the offtaker's stock returns. We also find an inverse relation between the rating upgrades of the offtaker and the spread paid by Quezon Power.

In risky public-private partnership (PPP) projects, governments and public institutions tend to offer private investors certain guarantees for their participation. However, when public sector capacity and institutions are weak, these guarantees can generate moral hazard in the bidding process and lead to contractual renegotiations, resulting in a loss for taxpayers. Drawing on a sophisticated, agent-based model that recreates the complex dynamics of the PPP procurement process, this paper demonstrates public sector competency is crucial for limiting moral hazard when guarantees are offered in PPP projects.

BACKGROUND: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. METHODS: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. FINDINGS: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammation and MBOAT7 genotype. Hepatic MBOAT7 levels were reduced in murine models of fatty liver, and by hyper-insulinemia. In wild-type mice, Mboat7 was down-regulated by refeeding and insulin, concomitantly with insulin signalling activation. Acute hepatic Mboat7 silencing promoted hepatic steatosis in vivo and enhanced expression of fatty acid transporter Fatp1. MBOAT7 deletion in hepatocytes reduced the incorporation of arachidonic acid into phosphatidylinositol, consistently with decreased enzymatic activity, determining the accumulation of saturated triglycerides, enhanced lipogenesis and FATP1 expression, while FATP1 deletion rescued the phenotype. INTERPRETATION: MBOAT7 down-regulation by hyper-insulinemia contributes to hepatic fat accumulation, impairing phosphatidylinositol remodelling and up-regulating FATP1. FUNDING: LV was supported by MyFirst Grant AIRC n.16888, Ricerca Finalizzata Ministero della Salute RF-2016–02,364,358, Ricerca corrente Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico; LV and AG received funding from the European Union Programme Horizon 2020 (No. 777,377) for the project LITMUS-"Liver Investigation: Testing Marker Utility in Steatohepatitis". MM was supported by Fondazione Italiana per lo Studio del Fegato (AISF) 'Mario Coppo' fellowship.