Wild food plants (WFP) have always been present in our kitchen, although they have not always been given the same importance as crops. In the Catalan linguistic area (CLA), covered in this paper, WFP were of great importance as a subsistence food not only during the years of the Spanish civil war (1936–1939) and World War II (1939–1945), but also long before these periods and in the years thereafter. The CLA has been well studied at the level of traditional knowledge on plant biodiversity, and much of this information is collected in a database by the EtnoBioFiC research group. The aim of this work is to carry out a meta-analysis of the WFP dataset of the CLA (only regarding edible uses, drinks excluded) and to identify the most quoted plants, and the information associated with them. With data from 1659 informants, we recorded 10,078 use reports of 291 taxa (278 of which at specific or subspecific levels and 13 only determined at generic level) belonging to 67 families. The most reported taxa, also with highest cultural importance indexes, are Thymus vulgaris, Foeniculum vulgare subsp. piperitum, Laurus nobilis, Rubus ulmifolius and Mentha spicata. The ethnobotanicity index for food plants is 6.62% and the informant consensus factor, also for food uses, is a very high 0.97, supporting the robustness of the information. The results provided and discussed in this work concern a significant part of the edible resources in the territory considered, which is, often and mainly, underestimated and underutilised. Its consideration could be an opportunity to promote closer and more sustainable agriculture. From the state-of-the-art of this question, it is possible to propose old, in some cases forgotten foods that could be newly introduced onto the market, first, but not only, at a local level, which could be interesting for new crop development in the frame of a valorisation of territorial identity.

Type 1 diabetes is an autoimmune condition caused by the lymphocyte-mediated destruction of the insulin-producing β cells in pancreatic islets. We aimed to identify final molecular entities targeted by the autoimmune assault on pancreatic β cells that are causally related to β cell viability. Here, we show that cyclin D3 is targeted by the autoimmune attack on pancreatic β cells in vivo. Cyclin D3 is down-regulated in a dose-dependent manner in β cells by leukocyte infiltration into the islets of the nonobese diabetic (NOD) type 1 diabetes-prone mouse model. Furthermore, we established a direct in vivo causal link between cyclin D3 expression levels and β-cell fitness and viability in the NOD mice. We found that changes in cyclin D3 expression levels in vivo altered the β-cell apoptosis rates, β-cell area homeostasis, and β-cell sensitivity to glucose without affecting β-cell proliferation in the NOD mice. Cyclin D3-deficient NOD mice exhibited exacerbated diabetes and impaired glucose responsiveness; conversely, transgenic NOD mice overexpressing cyclin D3 in β cells exhibited mild diabetes and improved glucose responsiveness. Overexpression of cyclin D3 in β cells of cyclin D3-deficient mice rescued them from the exacerbated diabetes observed in transgene-negative littermates. Moreover, cyclin D3 overexpression protected the NOD-derived insulinoma NIT-1 cell line from cytokine-induced apoptosis. Here, for the first time to our knowledge, cyclin D3 is identified as a key molecule targeted by autoimmunity that plays a nonredundant, protective, and cell cycle-independent role in β cells against inflammation-induced apoptosis and confers metabolic fitness to these cells.

BackgroundPancreatic islets are exposed to strong pro-apoptotic stimuli: inflammation and hyperglycemia, during the progression of the autoimmune diabetes (T1D). We found that the Cdk11(Cyclin Dependent Kinase 11) is downregulated by inflammation in the T1D prone NOD (non-obese diabetic) mouse model. The aim of this study is to determine the role of CDK11 in the pathogenesis of T1D and to assess the hierarchical relationship between CDK11 and Cyclin D3 in beta cell viability, since Cyclin D3, a natural ligand for CDK11, promotes beta cell viability and fitness in front of glucose.MethodsWe studied T1D pathogenesis in NOD mice hemideficient for CDK11 (N-HTZ), and, in N-HTZ deficient for Cyclin D3 (K11HTZ-D3KO), in comparison to their respective controls (N-WT and K11WT-D3KO). Moreover, we exposed pancreatic islets to either pro-inflammatory cytokines in the presence of increasing glucose concentrations, or Thapsigargin, an Endoplasmic Reticulum (ER)-stress inducing agent, and assessed apoptotic events. The expression of key ER-stress markers (Chop, Atf4 and Bip) was also determined.ResultsN-HTZ mice were significantly protected against T1D, and NS-HTZ pancreatic islets exhibited an impaired sensitivity to cytokine-induced apoptosis, regardless of glucose concentration. However, thapsigargin-induced apoptosis was not altered. Furthermore, CDK11 hemideficiency did not attenuate the exacerbation of T1D caused by Cyclin D3 deficiency.ConclusionsThis study is the first to report that CDK11 is repressed in T1D as a protection mechanism against inflammation-induced apoptosis and suggests that CDK11 lies upstream Cyclin D3 signaling. We unveil the CDK11/Cyclin D3 tandem as a new potential intervention target in T1D.