First developments towards closing the nutrient cycle in a biofuel production process

Hydrothermal liquefaction (HTL) of microalgae is a promising technology offering production of biofuels in a sustainable way. Thanks to the supercritical conditions applied, the recycling of water and nutrients including carbon capture becomes feasible1-2. Through HTL, the target bio-oil is generated together with process water containing valuable nutrients. In this study we have provided an environmentally friendly and resource efficient strategy to produce renewable microalgae biomass. Feasibility test on microalgae cultivation, using the nutrient-rich effluent from the HTL of same algal biomass, was performed in a 5L, flat panel airlift (FPA)-photobioreactor (PBR). 1g(DW) L-1d-1 of microalgae was the productivity average achieved with the diluted aqueous solution (25-fold). This is comparable to the productivity obtained with the standard growth medium even if an adaptation time of four days was necessary. Our results show that the nutrient rich HTL aqueous product of microalgal biomass conversion can replace to a great extent mineral salts of the culture medium. Together with an efficient water management, the nutrient recovery applied here promotes the recycling and prevents the release of waste materials and therefore shows the potential for driving the system towards a nutrient neutral production of biomass for biofuels

Androgen receptor overexpression in prostate cancer in type 2 diabetes.

Objective: While prostate cancer does not occur more often in men with diabetes, survival is markedly reduced in this patient group. Androgen signaling is a known and major driver for prostate cancer progression. Therefore, we analyzed major components of the androgen signaling chain and cell proliferation in relation to type 2 diabetes. Methods: Tumor content of 70 prostate tissue samples of men with type 2 diabetes and 59 samples of patients without diabetes was quantified by an experienced pathologist, and a subset of 51 samples was immunohistochemically stained for androgen receptor (AR). mRNA expression of AR, insulin receptor isoform A (IR-A) and B (IR-B) IGF-1 receptor (IGF1R), Cyp27A1 and Cyp7B1, PSA gene KLK3, PSMA gene FOLH1, Ki-67 gene MKI67, and estrogen receptor beta (ESR2) were analyzed by RT-qPCR. Results: AR mRNA and protein expression were associated with the tumor content only in men with diabetes. AR expression also correlated with downstream targets PSA (KLK3) and PSMA (FOLH1) and increased cell proliferation. Only in diabetes, AR expression was correlated to higher IR-AIIR-B ratio and lower IR-B/IGF1R ratio, thus, in favor of the mitogenic isoforms. Reduced Cyp27A1 and increased Cyp7B1 expressions in tumor suggest lower levels of protective estrogen receptor ligands in diabetes. Conclusions: We report elevated androgen receptor signaling and activity presumably due to altered insulin/IGF-1 receptors and decreased levels of protective estrogen receptor ligands in prostate cancer in men with diabetes. Our results reveal new insights why these patients have a worse prognosis. These findings provide the basis for future clinical trials to investigate treatment response in patients with prostate cancer and diabetes. 2017 The Authors. Published by Elsevier GmbH

TGFβ contributes to impaired exercise response by suppression of mitochondrial key regulators in skeletal muscle.

A substantial number of people at risk to develop type 2 diabetes could not improve insulin sensitivity by physical training intervention. We studied the mechanisms of this impaired exercise response in 20 middle-aged individuals at high risk to develop type 2 diabetes who performed a controlled eight weeks cycling and walking training at 80 % individual VO2peak. Participants identified as non-responders in insulin sensitivity (based on Matsuda index) did not differ in pre-intervention parameters compared to high responders. The failure to increase insulin sensitivity after training correlates with impaired up-regulation of mitochondrial fuel oxidation genes in skeletal muscle, and with the suppression of the upstream regulators PGC1α and AMPKα2. The muscle transcriptome of the non-responders is further characterized by an activation of TGFβ and TGFβ target genes, which is associated with increases in inflammatory and macrophage markers. TGFβ1 as inhibitor of mitochondrial regulators and insulin signaling is validated in human skeletal muscle cells. Activated TGFβ1 signaling down-regulates the abundance of PGC1α, AMPKα2, mitochondrial transcription factor TFAM, and of mitochondrial enzymes. Thus, the data suggest that increased TGFβ activity in skeletal muscle can attenuate the improvement of mitochondrial fuel oxidation after training and contribute to the failure to increase insulin sensitivity