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Volume 14 | August 2018

The lncRNA Blnc1 orchestrates adipose tissue remodeling to preserve metabolic healthBrown fat long noncoding RNA 1 (Blnc1) is a conserved long noncoding RNA (lncRNA) that is enriched in brown adipose tissue and promotes differentiation of cultured brown and beige adipocytes. Zhao et al. investigated the role of Blnc1 in adipose tissue remodeling. They found that fat-specific inactivation of Blnc1 accelerates brown fat whitening and impairs homeostatic fat expansion during a high-fat diet, leading to adipose tissue inflammation, insulin resistance and hepatic steatosis. Adipocyte-specific transgenic expression of Blnc1 elicited the opposite, beneficial metabolic effects. This shows a surprisingly powerful role of lncRNA in orchestrating adipocyte adaptation to obesity and maintaining systemic metabolic health.

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Three-dimensional volume imaging of vascular plasticity in adipose tissuesAdipose tissues are among the most highly vascularized organs of the body, with each adipocyte being in direct contact with capillaries. Intra-adipose vasculatures increase or decrease their density in response to various metabolic stimuli or stresses, a process known as vascular plasticity. Modulation of the vasculatures may exert significant and long-lasting effects on adipose metabolism. Cao, Wang et al. report a 3D volume fluorescence-imaging procedure to visualize the adipose vascular network at single-capillary resolution. To demonstrate the power of this imaging technique, they assess the pathological remodeling of vasculatures in adipose tissues under obese conditions and characterize the physiological changes of vasculatures in response to a cold challenge.

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Plasma N-Acylethanolamine levels as a biomarker of obesity and dysmetabolismN-acylethanolamines (NAEs) are bioactive lipids that are involved in a wide spectrum of processes, including inflammation, pain perception, and energy balance. Their exact role in determining, maintaining, and reflecting the obese status has not been clarified. Fanelli and colleagues tested the hypothesis that plasma NAE levels as well as their ratios are influenced by BMI and by menopause in women and ageing in men. Their results support the relevance of the NAE system as a target for interventions aiming at restoring metabolic health in humans.

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Pancreatic deletion of the IL-1 receptor disrupts glucose homeostasis and promotes β-cell de-differentiationThe interleuking-1 (IL-1) signaling system is associated with both acute and chronic inflammatory events. Inflammation is linked with reductions in β-cell function and mass in both type 1 and type 2 diabetes. Burke and colleagues studied the consequences of pancreatic IL-1 receptor deletion in mice. They found reduced glucose tolerance and insulin secretion, as well as signs of β-cell de-differentiation.

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Secretagogin protects Pdx1 from proteasomal degradation to control β cell specification Pancreatic and duodenal homeobox 1 (Pdx1) is a transcription factor that controls a transcriptional program which ultimately leads to the formation of functional β cells. It is, however, unknown how signal initiation by calcium is linked to the transcriptional effectors. Malenczyk et al. identify the Ca2+ sensor secretagogin as a protective factor for Pdx1 that acts by proteasome inhibition. By its action, a favorable α to β cell ratio is achieved in Langerhans islets.

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Hepatocyte TLR4 deficiency protects against alcohol-induced fatty liver diseaseEvidence suggests that inflammation is an essential factor contributing to the initiation and progression of alcoholic liver disease (ALD). Previous studies have shown that mutant toll-like receptor 4 (TLR4) mice, or mice deficient in TLR4, display attenuated alcohol-induced fatty liver disease, suggesting a direct role for TLR4 in the development of ALD. In this study, Jia et al. showed that selective TLR4 deletion from hepatocytes protects mice from chronic alcohol-induced liver injury and fatty liver.

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Specific subpopulations of LepR-expressing neurons mediate the effects of early LepR deletion on energy balanceThe hormone leptin, which is produced by adipose tissue to signal the repletion of fat stores, acts via its receptor (LepRb) on hypothalamic neurons to suppress food intake and permit energy expenditure. Leptin- or LepRb-deficient humans and rodent models display dramatic hyperphagia and reduced energy expenditure, leading to severe obesity. However, the specific LepRb neurons that mediate the largest component of this dramatic obesity phenotype remain undefined. Rupp et al. found that the early developmental deletion of LepRb from vGat or Nos1 neurons produced dramatic obesity, but deletion of LepRb from Pomc, Agrp, Ghrh, or Htr2c neurons minimally altered energy balance.

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PPARγ is dispensable for clear cell renal cell carcinoma progressionClear cell renal cell carcinoma (ccRCC), the most common subtype of kidney cancer, is characterized by robust intracellular lipid and glycogen accumulation. The peroxisome proliferator-activated receptor gamma (PPARγ) is the master regulator of adipogenesis. Sanchez and colleagues hypothesized that PPARγ promotes lipid storage in ccRCC and contributes to tumorigenesis, which they tested using loss-of-function experiments. PPARγ deletion in two ccRCC cell lines affected neither viability, proliferation, migratory capacity in vitro, nor tumor growth in a subcutaneous xenograft model. Surprisingly, PPARγ also appears to be dispensable for lipid storage and maintenance of total triglyceride levels in ccRCC cells.

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GIP is upregulated in patients with atherosclerosis and stabilizes plaques in ApoE-/- mice Glucose-dependent insulinotropic peptide (GIP) is secreted by enteroendocrine cells following nutrient intake leading to insulin secretion and glucose control. Kahles, Liberman et al. investigated the role of GIP in atherosclerotic cardiovascular disease with a focus on plaque morphology. They found elevated circulating GIP concentrations in patients with atherosclerosis and identified GIP as a vasoprotective peptide stabilizing atherosclerotic lesions in ApoE-/- mice by preventing monocyte migration and blocking proinflammatory activation of macrophages. Given that plaque erosion and rupture are critical steps in the process of myocardial infarction, these findings might open new therapeutic avenues for patients with high cardiovascular risk.

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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.



Jørgen Wojtaszewski, Janne Hingst
University of Copenhagen, Denmark
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