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The present review, to the authors' knowledge, is the first to specifically address the relationships between microcirculation and metabolic syndrome, a cluster of metabolic and cardiovascular modifications highly prevalent in the general population. Its close link to overweight and insulin resistance makes it the main cause of the worldwide burden of type 2 diabetes. However, metabolic syndrome is also observed in many other diseases, particularly, but not exclusively, those where insulin resistance is a main feature. Analysis of the literature reveals that this clinical situation is invariably linked to microvascular disturbances, such as abnormalities in arteriolar reactivity, capillary recruitment, permeability, and hemorheology. A particularly interesting observation is that these defects in small vessel structure and function are seen very early in life or disease. Very importantly, they further suggest that microcirculatory abnormalities may be not only secondary but also causal to the development and/or aggravation of insulin resistance and metabolic syndrome. Mechanisms responsible for these modifications remain largely unknown, but insulin's vascular effects in the microvascular network, detailed in this review, are at least one example of such connections. The existing data point to a clear, at least bidirectional, relationship between microcirculation and metabolic syndrome. Additional studies should determine the level of reciprocal causality. [ABSTRACT FROM AUTHOR]

Epidemiological studies have linked obesity during pregnancy to an increased risk of developing metabolic syndrome (MetS) for the progeny. The aim of our current work is, therefore, to study, in a rat model, how maternal Diet-Induced Obesity (DIO) can program the development of MetS in the offspring. We developed a DIO model in which female Wistar rats are rendered obese by consuming, from weaning on, a diet enriched in fat and/or sucrose (OB1: 45%kcal fat, 15.5%kcal sucrose, and OB2: 45%kcal fat+sweetened condensed milk). A group of control females fed lab chow (C) was also included. At 3 months of age (body weights: C=256±7g, OB1=292±17g and OB2=305±14g), females were mated and allowed to deliver spontaneously. At 21 days of age, offspring were weaned onto usual lab chow diet. OB1 (male only) and OB2 (male and female) offspring presented an increased body weight gain when compared to C offspring. Food intake was also increased. Oral glucose tolerance tests performed in 3 months-old offspring showed that glucose tolerance was reduced in the OB2 offspring (males and females). Preliminary data of the hyperinsulinemic–euglycemic clamps demonstrated a lower insulin sensitivity as well. At 6 months of age, body composition was determined, showing that OB1 and OB2 offspring were significantly fatter than the C offspring. Basal insulin and leptin levels were also increased. Taken together, our results support the hypothesis that maternal DIO programs the development of MetS in the offspring. [Copyright &y& Elsevier]