MicroRNAs (MiRNAs) are small RNA molecules that can exert regulatory functions in gene expression. MiRNAs have been identified in diverse tissues and biological fluids, both in the context of health and disease. Breastfeeding has been widely recognized for its superior nutritional benefits; however, a number of bioactive compounds have been found to transcend these well-documented nutritional contributions. Breast milk was identified as a rich source of miRNAs. There has been increasing interest about their potential ability to transfer to the offspring as well as what their specific involvement is within the benefits of breast milk in the infant. In comparison to breast milk, formula milk lacks many of the benefits of breastfeeding, which is thought to be a result of the absence of some of these bioactive compounds. In recent years, the miRNA profile of breast milk has been widely studied, along with the possible transfer mechanisms throughout the infant’s digestive tract and the role of miRNA-modulated genes and their potential protective and regulatory functions. Nonetheless, to date, the current evidence is not consistent, as many methodological limitations have been identified; hence, discrepancies exits about the biological functions of miRNAs. Further research is needed to provide thorough knowledge in this field.

Summary: Mutations in hepatocyte nuclear factor 1β gene ( HNF1B ) are responsible for a multisystemic syndrome where monogenic diabetes (classically known as MODY 5) and renal anomalies, mostly cysts, are the most characteristic findings. Urogenital malformations, altered liver function tests, hypomagnesemia or hyperuricemia and gout are also part of the syndrome. Diabetes in these patients usually requires early insulinization. We present the case of a young non-obese male patient with a personal history of renal multicystic dysplasia and a debut of diabetes during adolescence with simple hyperglycemia, negative pancreatic autoimmunity and detectable C-peptide levels. He also presented epididymal and seminal vesicle cysts, hypertransaminasemia, hyperuricemia and low magnesium levels. In the light of these facts we considered the possibility of a HNF1B mutation. The sequencing study of this gene confirmed a heterozygous mutation leading to a truncated and less functional protein. Genetic studies of his relatives were negative; consequently, it was classified as a de novo mutation. In particular, our patient maintained good control of his diabetes on oral antidiabetic agents for a long period of time. He eventually needed insulinization although oral therapy was continued alongside, allowing reduction of prandial insulin requirements. The real prevalence of mutations in HNF1B is probably underestimated owing to a wide phenotypical variability. As endocrinologists, we should consider this possibility in young non-obese diabetic patients with a history of chronic non-diabetic nephropathy, especially in the presence of some of the other characteristic manifestations. Learning points: HNF1B mutations are a rare cause of monogenic diabetes, often being a part of a multisystemic syndrome. The combination of young-onset diabetes and genitourinary anomalies with slowly progressive nephropathy of non-diabetic origin in non-obese subjects should rise the suspicion of such occurrence. A family history may not be present. Once diagnosis is made, treatment of diabetes with oral agents is worth trying, since the response can be sustained for a longer period than the one usually described. Oral treatment can help postpone insulinization and, once this is necessary, can help reduce the required doses.