The intracellular transport of glucose into fat cells (adipocytes) after a meal is dependent on insulin. Insulin induces glucose uptake, promotes the building of adipose tissue (lipogenesis), while inhibiting the breakdown of fat cells (lipolysis), and thus the release of free fatty acids into the bloodstream. It is estimated that adipose tissue accounts for approximately 10% of insulin-stimulated glucose uptake in the whole body.
In the basic state (not the post-meal state and not the state of starvation) adipocytes are not dependent on glucose, intracellular energy can be supplied as a result of fatty acid oxidation in insulin deficiency. At the same time, free fatty acids are released into the circulation for their direct use by other organs, e.g. in the heart or in the liver, where they are converted into ketone bodies. Ketone bodies are an alternative energy substrate for the brain during prolonged starvation.
With insulin resistance, the processes occurring in adipose tissue are similar, with the increased flow of free fatty acids in the liver inducing the production of very low-density lipoproteins (VLDL). Ketogenesis is then inhibited by compensatory hyperinsulinemia. In addition, since lipoprotein lipase activity is insulin-dependent, and in the insulin-resistant state, lipase activity is impaired, peripheral triglyceride uptake from VLDL is also reduced. These mechanisms contribute to the observed hypertriglyceridemia (high levels of triglycerides). In addition to free fatty acids, adipose tissue secretes a number of cytokines (proteins that stimulate other cells of the immune system to react in certain ways) that have a systemic effect on insulin resistance.
Source: Wilcox G.. Clin Biochem Rev. 2005 May;26(2):19-39. PMID: 16278749; PMCID: PMC1204764.