Hernandulcin (HE) is a non‐caloric sweetener synthesized by the Mexican medicinal plant Phyla scaberrima. Herein we present the results of HE production through cell suspensions of P. scaberrima as well as the influence of pH, temperature, biosynthetic precursors and potential elicitors to enhance HE accumulation. The incorporation of mevalonolactone (30–400 mg L−1) farnesol (30–400 mg L−1), AgNO3 (0.025–0.175 M), cellulase (5–60 mg L−1; 0.3 units/mg), chitin (20–140 mg L−1) and (+)‐epi‐α‐bisabolol (300‐210 mg L−1) to the cell suspensions, resulted in a differential accumulation of HE and biomass. Among elicitors assayed, chitin, cellulase and farnesol increased HE production from 93.2 to ∼160 mg L−1 but, (+)‐epi‐α‐bisabolol (obtained by a synthetic biology approach) increased HE accumulation up to 182.7 mg L−1. HE produced by the cell suspensions was evaluated against nine strains from six species of gastrointestinal bacteria revealing moderate antibacterial activity (MIC, 214–465 μg mL−1) against Staphylococcus aureus, Escherichia coli and Helicobacter pylori. Similarly, HE showed weak toxicity against Lactobacillus sp. and Bifidobacterium bifidum (>1 mg mL−1), suggesting a selective antimicrobial activity on some species of gut microbiota. According to our results, chitin and (+)‐epi‐α‐bisabolol were the most effective molecules to enhance HE accumulation in cell suspensions of P. scaberrima.

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The gene system of transcytosis, integrated by LRP2, AMN, CUBN, ARH, AMN and CUBN, might be important for the treatment and monitoring of chronic complications of diabetics, as well as for drug interactions, since they mediate the reuptake of vitamins such as B complex, folic acid and lipoproteins, which are closely related to the progression of diabetes. That is why polymorphisms in those genes could be targets of personalized medicine, to improve the quality of health care. It is important for both the clinical researcher and physician to explore new personalized treatment options for better care of the diabetic patient. The search for genetic or genomic markers in order to predict complications of disease, progression as well as to evaluate the therapeutic response to drugs and the presentation of adverse effects is an area to be explored, considering the high costs that represent the attention of diabetics to hospitals from the public sector. Other reasons are that type 2 diabetes mellitus (T2D) patients develop complications related with the progression of the disease, as well as, adverse and side effects resulting from drug interactions [1,2]. T2D commonly presents deficiency of vitamin B complex, associated with the long-term consumption of metformin. The consequences of this deficiency are increased cardiovascular risk, renal damage and higher risk of peripheral neuropathy and senile dementia [1,2]. Additionally, the chronic consumption of statins for the control of hypercholesterolemia and cardiovascular risk results in secondary dyslipidemia myocytes inflammation [1,2].The common element that might explain the previously described complications and side effects in T2D diabetic patients is an axis of genes that encode for the system of transcytosis in the cellular membranes from small intestine, kidney, liver, striated muscle, and other tissues. The components of this transcytosis system are LRP2, AMN, CUBN, ARH, Dab2, GIPC, NHE3, ClC5, FcRn and NaPi-IIa, which mediate the reuptake of B complex vitamins, including folic acid among other molecules [3][4][5][6][7][8][9][10].The clinical effect of these genes might be seen in the development of different diseases or clinical conditions (Table 1). Mutations in LRP2 have been associated with diabetes, aminoglucosides response, DonnaiBarrow syndrome (DBS), Facio-oculo-acoustic-renal syndrome (FOAR) and Alzheimer's disease. While mutations in AMN and CUB occur with megaloblastic anemia plus albuminuria. CUBallelic variants are related to the progression of renal damage and ARH variations are associated with hypercholesterolemia [3][4][5][6][7][8][9][10]. NHE3 mutations show association with congenital sodium diarrhea, whereas ClC5 gene is related to renal failure or Dent disease. ClC5, FcRn, NaPi-IIa gene are related with metabolic renal disease. DAB2, GIPC has an uncertain meaning in human pathology, but their pathogenic effect must be explored [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25].Considering the interaction between these genes...

Diabetes mellitus type 2 (DM2) is a worldwide public health problem. The etiology of the disease is multifactorial and is characterized by great heterogeneity of metabolic disorders. The most common are the insufficient production of insulin, insulin resistance and impaired incretin system. The specialist must understand the multi-causal nature of DM2 in the post-genomic era. This nature is determined by the additive effect of genes and environment, so there is no simple genetic epidemiological model to explain the inheritance pattern. Hence the need to establish the proportion of disease that is determined by genes and the contribution of environmental factors, the combination of which regulates the threshold or tolerance level for diabetes development. Given this complexity in DM2 in this work are discussed the various existing theories of causality of this disease, which will permit us to understand the interaction between the environment and the human genome, and also to know how risk factors or predisposition to this disease influence, laying the grounds that delimit environment interaction with the genome.