Recent technological developments have allowed determination of the age of fat cells and their lipids in adult humans. In contrast to prior views, this has demonstrated a high turnover rate of the fat cells (10%/year) and their unilocular lipid droplets (six times/10 years). Fat cell turnover is increased in obesity and when adipose tissue is composed of many but small adipocytes (hyperplasia, a benign adipose phenotype). While fat mass gain increases adipocyte number and size, only the latter is altered (decreased) after weight loss, which may facilitate weight regain. Fat cell lipid turnover is attenuated in subjects with excess body fat. In the subcutaneous region, this dysregulation occurs already in the overweight state while in the visceral depot, it is only observed in severe obesity. This may explain why the latter depot is particularly pernicious in the overweight/obese state as it allows for more rapid lipid fluxes between visceral fat and the liver. Adipose lipid turnover decreases during ageing due to impaired breakdown (lipolysis) of stored triglycerides. If this decline is not compensated by reduced adipocyte lipid uptake, bodyweight will increase over time. In concordance with this, low lipolysis rates are a risk factor for future weight gain and glucose intolerance. Adipose lipid turnover is also decreased in insulin resistance and certain forms of dyslipidemia. Altogether, adult human adipose tissue is in a highly dynamic state. Alterations in the turnover of fat cells and their lipids are therefore novel factors to consider in the pathophysiology of common metabolic disorders.
Keywords: adipocyte; dyslipidemia; fatty acids; obesity; type 2 diabetes mellitus.
© 2021 The Authors. Journal of Internal Medicine published by John Wiley & Sons Ltd on behalf of Association for Publication of The Journal of Internal Medicine.