ABSTRACT
Since 1964, the hypothesis of Pedersen has been used to explain fetal macrosomia observed in gestational diabetes mellitus (GDM), by a mechanism involving maternal hyperglycemia - fetal hyperglycemia - fetal hyperinsulinemia. However,since the 1980-89 decade, it is known that pregnant women with pre-gestationaloverweight not suffering from GDM still have a higher frequency of fetal macrosomia. Furthermore, pregnant women with GDM, despite being subjected to optimalglycemic control, still show unacceptably high frequencies of fetal macrosomia, aphenomenon that is concentrated in pregnancies with overweight or obesity priorto pregnancy. If glucose is not the single nutrient responsible for fetal macrosomiain pregnant women with gestational diabetes that undergo strict glycemic control,other nutrients may cause excessive fetal growth in pre-pregnancy overweightmothers. In this review, we propose that triglycerides (TG) could be responsible forthis accelerated fetal growth. If this hypothesis is validated in animal models andclinical studies, then normal and pathological ranges of TG should be defined, andmonitoring of triglyceride levels during pregnancy should be advised as a possiblenew alternative, besides a good glycemic control, for the management of fetal macrosomia in GDM women with overweight prior to pregnancy.
Subject(s)
Female , Humans , Infant, Newborn , Pregnancy , Diabetes, Gestational/blood , Fetal Macrosomia/etiology , Hyperglycemia/complications , Hypertriglyceridemia/complications , Triglycerides/blood , Blood Glucose/physiology , Gestational Age , Glucose Tolerance Test , Hypertriglyceridemia/blood , Obesity/complications , Overweight/etiologyABSTRACT
Nowadays, Diabetic Neuropathy (DN) is considered the most common cause of peripheral neuropathy in clinical practice. It can affect sensitive, motor or autonomic nerve fibers, with symmetric, asymmetric, acute or chronic presentations. Due to this variability, with multiple physiopathologic mechanisms involved, a complex clinical classification has been used until recently. The aim of this review is to present a new classification of diabetic neuropathy, based on its physiopathology. It is divided in metabolic microvascular and hypoxic, autoimmune and inflammatory, compressive, secondary to complications ofdiabetes and related to treatment. It must be understood that DN is notjust a functional disease, but a complication of diabetes with molecular and pathological substrates caused by hyperglycemia. Therefore, normalization of blood glucose is a fundamental step towards the successful prevention and treatment of DN.