Featured Articles

Volume 19 | January 2019

SGLT1 in pancreatic α cells regulates glucagon secretion Pancreatic α cells secrete glucagon, which controls blood glucose levels. In patients with type 1 or type 2 diabetes, hyperglycemia is often associated with hyperglucagonemia. However, the mechanism underlying excessive glucagon secretion is not fully understood. A recent report described the expression of sodium glucose cotransporters (SGLT) 1 and 2 in α cells. Suga et al. suggest that a novel mechanism regulates glucagon secretion through SGLT1 in α cells. Their findings might have implications for the classification and selection of SGLT2 inhibitors in the treatment of diabetes.

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Diacylglycerol kinase is a regulator of insulin secretionObesity is a complex disorder involving many genetic and environmental factors that are required to maintain energy homeostasis. Trinh et al. performed a large-scale in vivo screen for obesity-associated genes in Drosophila neurons. They identified 24 genes, including genes that have been previously associated with energy homeostasis in flies. One of the genes identified was Diacylglycerol kinase (Dgk), the homologues of which have been associated with obesity in human populations and have been shown to regulate insulin secretion in vitro. The authors performed the first functional study of Dgk in flies and showed that it is involved in lipid and carbohydrate metabolism.

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Moderate weight loss attenuates endoplasmic reticulum stress and mitochondrial dysfunction Endoplasmic reticulum (ER) stress and mitochondrial dysfunction seem to play a role in obesity and might be interesting as therapeutic targets. López-Domènech and colleagues assessed the effect of moderate weight loss in obese individuals on ER and mitochondrial function. Interestingly, the improvement in systemic inflammation and glucose tolerance was mirrored by an attenuation of chronic ER stress and mitochondrial dysfunction and was accompanied by enhanced expression of chaperones and antioxidants.

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Tannic acid, a histone acetyltransferase inhibitor, prevents non-alcoholic fatty liver disease Non-alcoholic fatty liver disease (NAFLD) development is influenced by environmental as well as genetic factors. The environment influences gene expression by altering histone acetylation patterns in the chromatin, which is regulated by histone acetyltransferases (HATs) and deacetylases. Chung et al. identified tannic acid as a novel HAT inhibitor and demonstrated that tannic acid prevented the development of NAFLD via its HAT inhibition activity, both in vitro and in vivo.

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GPR142 controls metabolism through regulation of pancreatic and gut hormonesGPR142 is a G protein coupled receptor that is almost exclusively expressed in the islets of the pancreas. Our knowledge about its physiological role and pharmacological potential is very limited. Rudenko and colleagues discovered that GPR142 efficiently stimulates pancreatic glucagon secretion and found that the effect of GPR142 agonism on glucose disposal is a balance between insulin-mediated glucose uptake in fat and muscle and glucagon-mediated glucose production in the liver. Surprisingly, GPR142 agonism also increased energy expenditure and improved insulin sensitivity.

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Fibroblast activation protein is dispensable for glucose homeostasis and body weight Fibroblast activation protein (FAP) has over 50% sequence identity with dipeptidyl peptidase-4 (DPP-4). The therapeutic success of DPP-4 inhibitors for the treatment of type 2 diabetes has stimulated interest in the metabolic actions of FAP. Panaro and colleagues found that Fap-/- mice did not exhibit improved glucose control or resistance to weight gain after prolonged high fat feeding. Their findings indicate that murine FAP is not a critical determinant of islet function, glucose homeostasis, weight gain, and the metabolic response to high fat feeding in mice.

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CPT1C in the hypothalamus is necessary for brown fat thermogenesis activationCarnitine palmitoyltransferase 1 isoform C (CPT1C) is located in the endoplasmic reticulum of hypothalamic neurons. It is able to bind malonyl-CoA, suggesting that it could act as a sensor of this lipid intermediary. CPT1C knockout (KO) mice are more prone to become obese when chronically fed a high fat diet with a reduced peripheral fatty acid oxidation. Rodríguez-Rodríguez et al. show that the obese phenotype and metabolic inflexibility that characterizes CPT1C KO mice is related to an impaired brown adipose tissue thermogenesis. Thus, their data uncover CPT1C as a key factor in the control of brown fat thermogenesis.

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Function of the extracellular matrix proteoglycan Lumican in obesity and glucose homeostasisAdipose tissue expansion in the face of caloric excess initiates processes including angiogenesis, inflammation, and extracellular matrix (ECM) remodeling. The small leucine-rich proteoglycan Lumican, a component of the ECM, binds collagen and is associated with repair processes in collagen-rich connective tissues. Wolff et al. explored the impact of Lumican loss and over-expression on metabolism and adipose tissue. They observed a sex-specific effect on fat accumulation in female Lumican knockout mice that coincided with increased inflammation and insulin resistance. Likewise, Lumican overexpression in the visceral fat and liver improved glucose clearance and insulin sensitivity.

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The 60 Second Metabolist
In this section authors briefly report on their work recently published in Molecular Metabolism.

Watch the most recent interview by clicking the video still. The link "referring article" directs you to this author's publication.



Amna Khamis
University of Lille, CNRS, Institute Pasteur de Lille, Lille, France
Referring article

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