Postprandial consequences of lipid absorption in the onset of obesity: Role of intestinal CD36.

Obesity has reached epidemic proportions and its incidence is still increasing. Obesity is an excess of fat, which can have harmful consequences such as inflammation, insulin resistance or dyslipidemia. Taken together, these conditions are known as metabolic syndrome (MetS).

Decrease in αβ/γδ T-cell ratio is accompanied by a reduction in high-fat diet-induced weight gain, insulin resistance, and inflammation.

The implication of αβ and γδ T cells in obesity-associated inflammation and insulin resistance (IR) remains uncertain. Mice lacking γδ T cells show either no difference or a decrease in high-fat diet (HFD)-induced IR, whereas partial depletion in γδ T cells does not protect from HFD-induced IR. αβ T-cell deficiency leads to a decrease in white adipose tissue (WAT) inflammation and IR without weight change, but partial depletion of these cells has not been studied.

Appetite control by the tongue-gut axis and evaluation of the role of CD36/SR-B2.

Understanding the mechanisms governing food intake is a public health issue given the dramatic rise of obesity over the world. The overconsumption of tasty energy-dense foods rich in lipids is considered to be one of the nutritional causes of this epidemic. Over the last decade, the identification of fatty acid receptors in strategic places in the body (i.

Obesogen effects after perinatal exposure of 4,4'-sulfonyldiphenol (Bisphenol S) in C57BL/6 mice.

Bisphenol A were removed from consumer products and replaced by chemical substitutes such as Bisphenol S (BPS). Based on their structural similarity, BPS may be obesogen like Bisphenol A in mice. Our objective was to determine the impact of BPS on lipid homeostasis in C57Bl/6 mice after perinatal and chronic exposure.