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Metformin is the most widely used oral antidiabetic agent for the treatment of type 2 diabetes (T2D) and the association of the use of this drug with vitamin B12 deficiency has been described. A review of studies was carried out to find out the evidence of this association and the recommendations for its detection, prevention and treatment. The reported prevalence of vitamin B12 deficiency in patients treated with metformin ranged from 5.8% to 52% in the different series. Older patients, those who received metformin at high doses and for a longer time, and those who do not consume food of animal origin, are those who are at greater risk of suffering from this deficit.

Introduction: the prolonged use of metformin and the lack of consumption of vitamin B12 can cause its deficit, in T2D. Objectives: to analyze the frequency of insufficient consumption of vitamin B12 according to: personal characteristics, anthropometric and laboratory data, and use of metformin; associate serum cobalamin levels with metformin dose and time; establish a relationship between B12 intake and serum levels. Materials and methods: cross-sectional design. Through a survey of the frequency of consumption of food sources of B12 in 200 patients treated with metformin for more than 18 months. Clinical, anthropometric, laboratory data, time and dose of metformin were analyzed in 2 health centers in the Province of Buenos Aires. Results: the percentage of de cient consumption was 29%. 47.5% of unemployment was registered, which reached an in-take deficit of 32.6%. Serum B12 was measured in 65% of the sample where 53.8% of values were abnormal (0.8% in deficient levels) and 23% at levels normal lower cut-off point, with a significant association being observed at doses of metformin ≥1,500 mg. Deficiencies in B12 intake (

Preemptive, early-life strategies beginning in utero that reduce risk for childhood obesity are imperative to arrest the intergenerational cycle of diabetes and metabolic disease including childhood obesity and non-alcoholic fatty liver disease (NAFLD). Metabolic factors as well as drugs that cross the placenta can create an intrauterine environment with profound effects on prenatal development and enhanced susceptibility to later chronic disease. In the first part of this talk we take a close look at metformin, widely used to treat GDM but an agent in which fetal concentrations are higher than maternal and concentrated 1000-fold in fetal and placental mitochondria due to organic cation transporters. We review metformin’s multitude of intracellular effects including its anticancer effects, growth inhibitory properties, and suppression of mitochondrial respiration. We also review data from the Metformin in Gestation (MiG) and PCOS RCTs which randomized pregnant women to metformin, and which found an increased risk of childhood overweight at 5-10 years1,2. We will discuss how the growth inhibiting properties of metformin appear to increase the risk for small-for-gestational-age (SGA) infants, also a risk factor for subsequent childhood obesity, demonstrated recently in the MiTY RCT in which metformin was added to insulin for Type 2 diabetes.

Introduction: Obesity is a serious health issue worldwide. Feeding habits and stress are among the environmental factors that contribute to its development. Additionally, it’s been described an association between obesity and cognitive function, being pointed as a risk factor for Alzheimer’s disease. Objectives: To study the effect of a high-fat diet (HFD) consumption and the development of cognitive deficit. To evaluate whether the exposition to chronic mild stress aggravates the metabolic and/or cognitive disorders induced by the HFD. Furthermore, being the metformin (MET) a drug commonly used to treat diabetes, we will study its effects on behavior. Methodology: One month old, Male C57Bl/6J mice were fed with a standard diet (SD; 2.96 kcal/g) or a high-fat diet (HFD; 4.37 kcal/g) during 28 weeks. At the 8th week of diet, animals were divided and a group of each diet were chronically exposed to random mild stressors (CMS). After 12 weeks of diet, a group of animals under each treatment were given MET (250 mg/kg*day). We studied the glucidic (basal glycemia, glucose tolerance, insulinemia) and lipidic metabolism (total cholesterol, HDL cholesterol, triglycerides) and we studied the behavior (learning, spatial memory, working memory).

Symposium 19: Drug Treatment: What's New? Insulinosensitizers: metformin and TZD Metformin represents a striking example of “historical nemesis” of a drug. Currently, despite the arrival of new innovative drugs, metformin still stands as a first choice drug for T2D. Several effects are attributed to metformin, apart from hypoglycemic action, weight loss, cardiovascular and kidney protection, beneficial actions over different types of cancer, decrease of liver diseases, actions to reduce aging effects, etc. Metformin is a multifaceted drug, with multiple action and molecular mechanisms. It inhibits the mitochondrial complex I, which leads to AMPK activation. It also reduces glucose levels through GLUT-4 increase. It is one of the few oral agents that prevents weight increase or even favors weight loss in patients with T2D, because of the gut flora modification and the modulation of the hypothalamic appetite regulation. It also stimulates thermogenesis.

Introduction: Hyperglycemia is one of the most important factors that determine the production of oxidative stress and inflammation, processes that can accelerate telomere shortening. Objectives: The objectives were to analyse the absolute telomere length (aTL) in individuals with altered fasting glucose levels (AFG) compared to individuals with normal glucose levels (NFG). To study from a prospective controlled study, the variation in aTL in patients with decompensated type 2 diabetes (T2D) before and after treatment. Materials and Methods: A population of 246 individuals of both genders was studied, which were divided into a group of individuals with blood glucose levels 50Y). A subgroup of 30 patients with newly diagnosed T2D was studied, at the beginning (T0), and at 6 months (T6) of a pharmacological treatment and hygienic-dietary measures with the objective of achieving metabolic compensation. In both studies, the biochemical-clinical variables of all individuals and the aTL were determined by quantitative real-time PCR. Statistical analyses were performed using Graph Pad Prism and SPSS software.

Introduction: the regulation of glycemia requires the activation of different hormones in addition to insulin. Through mechanisms of insulinopenia or insulin resistance (IR), as in acromegaly (Acro) or Cushing's syndrome, endocrinopathies can precipitate states of hyperglycemia. The presence of diabetes mellitus (DM) increases the morbidity and mortality of these patients, which is why both the treatment and follow-up of the underlying disease is fundamental. Objectives: to describe the clinical and biochemical characteristics of patients with Acro and hypercortisolism (HyperC), comparing those with or without DM.