Obesity is a metabolic, multifactorial disease that is underpinned by factors such as genetics, epigenetics, as well as high-energy food intake and sedentarism. Obesity is often associated with, and exacerbated by, other metabolic disorders such as type 2 diabetes mellitus (T2DM). A hallmark of T2DM is failure of insulin secretion from pancreatic β-cell to regulate blood glucose disposal into peripheral tissues, such as skeletal muscle, termed insulin resistance, as well as deregulation of pancreatic α-cell function. It has been proposed that insulin resistance is, in part, a consequence of impaired signal transduction of insulin caused by several molecules released from adipose tissue that include (adipo)cytokines and fatty acids. However, not all fatty acids exert a negative impact on insulin sensitivity. In fact, it has been suggested that palmitoleic acid (16:1n-7) has hormone-like properties and improves some metabolic parameters that are impaired in obesity and T2DM. Moreover, in vitro approaches reveal that cis-16:1n-7 can influence pancreatic β-cell survival, insulin secretion, and skeletal muscle insulin response and adipocyte metabolism. In vivo experiments using animal models show that the ingestion of cis-16:1n-7 or sources of it (e.g., macadamia oil) can partially prevent the metabolic alterations caused by high-fat/carbohydrate diets. In general, studies in humans found positive associations between higher trans-16:1n-7 proportion in plasma phospholipids and improved insulin sensitivity or decreased the onset of T2DM. However, plasma cis-16:1n-7 data are still controversial. In this brief review, we discuss the main studies on 16:1n-7 effects on obesity and T2DM and their potential for clinical application.
Keywords: Diabetes; glucose homeostasis; insulin sensitivity; obesity; omega-7; palmitoleic acid.
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