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mice . Nature 382 448 – 452 . Ferron M Hinoi E Karsenty G Ducy P 2008 Osteocalcin differentially regulates beta cell and adipocyte gene expression and affects the development of metabolic diseases in wild-type mice . PNAS 105 5266

proliferator-activated receptor (PPAR) α in the liver ( Badman et al . 2007 ) and PPARγ in the adipocytes ( Wang et al . 2008 ). Several clinical studies investigated the role of FGF21 in human metabolic disease. Thus, high baseline FGF21 serum levels

exert the same inhibitory action on intestinal FXR. BA metabolism in constipation and possible link to metabolic diseases The interrelationship between BA homeostasis and metabolic diseases is far more complex. For example, it is known that patients with

commonly used products. Recently, growing evidence has indicated that exposure to BPA is associated with an increased risk of some metabolic diseases such as obesity, insulin resistance, type 2 diabetes, dyslipidemia, etc. ( Alonso-Magdalena et al . 2011

, adipokines mediate physiological functions while in states of metabolic disease the adipokines have altered effects, modulating insulin resistance either directly by affecting the insulin signalling pathway or indirectly via stimulation of inflammatory

system and metabolism. Changes in immune cell populations and immunological messengers (i.e. cytokines) have been implicated in the pathogenesis of metabolic disease and can alter blood glucose, insulin, and insulin resistance during obesity

mechanisms by which excess FA availability is thought to reduce insulin action in muscle and predispose to metabolic diseases. Fuel for energy production All three of the major types of macromolecules that make up organic material (carbohydrates, proteins and

insulin resistance. So how does the maternal pancreas cope with the sustained insulin demand of pregnancy? Pancreatic β-cells are plastic and can respond to changes in insulin demand and, although this is pathological in metabolic diseases, this same

al. 2013 ). In addition, the incidence of metabolic diseases and their co-morbidities is sexually dimorphic, and varies depending on the gonadal status; for example, increases after menopause ( Mauvais-Jarvis 2015 ). However, the influence of

metabolic risk factors for CAD seem to promote the production of monocytes through varying mechanisms. While these risk factors act through independent pathways, it is important to note that these risk factors typically cluster together in metabolic diseases