Cells articles from across Nature Portfolio

Obesity is a risk factor for diseases. Here, authors found that inhibition of cyclin-dependent kinase 6 increased de novo lipogenesis in the adipose tissues but not in the liver, which may provide a strategy to concur obesity-induced maladies.

Zhang et al. show that in mice, an adipocyte population with high expression of the transcription factor JunB in the brown adipose tissue shows reduced thermogenic capacity. Depletion of JunB increases the fraction of adipocytes with high thermogenic capacity and ameliorates diet-induced insulin resistance.

Lipolysis in adipose tissue releases fatty acids during fasting. Here, authors show that ApoL6, a lipid droplet-associated protein, is specifically expressed in adipocytes upon feeding to inhibit lipolysis by directly interacting with Perilipin 1 to competitively inhibit Perilipin 1-HSL interaction.

This Review examines the origins of marrow adipocytes and their function under normal or pathological conditions. Regulation of bone marrow adipose tissue by nutrient status is considered, as well as the interactions between bone marrow adipose tissue, haematopoietic cells of the bone marrow and the bone.

A new study by Reverte-Salisa and colleagues identifies a molecular mechanism through which the cAMP-mediating protein EPAC1 controls the size of brown and beige adipose tissue. This finding opens the door for the development of pharmacological interventions to prevent the decline of brown adipose tissue in obesity and ageing, and thereby improve metabolic health.

Schuermans et al. report phospholipase A and acyltransferase 3 (PLAAT3) deficiency in patients with lipodystrophy and peripheral neuropathy. Their discovery adds to the growing list of genetic lipodystrophies due to deficiencies of enzymes involved in phospholipid biosynthesis, including 1-acylglycerol-3-phosphate O-acyltransferase 2 and choline phosphate cytidylyltransferase 1 A.