Just a few quotes from scientific articles. I found them suggestive.
Adipose tissue lipolysis and free fatty acid release into plasma are exquisitely sensitive to insulin and half-maximal suppression of lipolysis occurs within the range of normal fasting plasma insulin concentrations
Fat mobilization is suppressed rapidly by insulin. Plasma NEFA concentrations therefore fall after any meal that contains carbohydrates, which stimulate insulin release. Spillover fatty acids somewhat reduce this effect but do not override it. Circadian profiles of plasma NEFA concentrations therefore show the highest concentrations after an overnight fast, with suppression after each meal
adipose tissue is a net importer of dietary fat for 5 h following a single test meal and for most of the day during a typical three-meal eating pattern
Over the 24 h period, there was net uptake of fatty acids immediately after the first meal, and this continued until approximately 17 h after breakfast, i.e. during the whole of the daytime adipose tissue takes up and stores fatty acids.
These observations do raise the intriguing possibility of differential nutritional regulation of lipogenesis. In the fasting state, low insulin levels and high endogenous GC levels will stimulate lipolysis and simultaneously switch off lipogenesis though serine phosphorylation of ACC1, decreasing fuel storage and increasing FFA availability for other more metabolically active tissues. Conversely, in the fed state, insulin levels are high, and here insulin and GC may act together to promote lipid storage.
The AT triglyceride content depends primarily on the balance between lipogenesis and lipolysis, two opposing processes regulated by a complex interaction of several factors including circulating hormones, such as insulin, as well as by adipose-derived factors, such as leptin and adiponectin, which in turn have an important role on insulin action
Refeeding attenuates adipocyte lipolysis, primarily through the potent antilipolytic actions of insulin. This regulatory pathway has also been studied and reviewed extensively. Rapid, acute regulation of lipolysis by insulin involves both cAMP-dependent and cAMP-independent mechanisms.
Regulation of TAG synthesis in AT is stimulated by insulin at multiple stages; the net effect of insulin on TAG stores is strongly ‘anabolic’.
Lipolysis and fat mobilization is also under powerful inhibitory control by various hormones and secreted factors. Fat mobilization is potently suppressed by insulin acting through its usual signalling pathway for the control of acute metabolic events, that is, through phosphatidylinositol-3′-kinase and protein kinase B activation, which in turn phosphorylates and activates phosphodiesterase 3B, which hydrolyses cAMP to AMP and reduces the lipolytic activity.
Insulin signalling is uniquely required for storing energy as fat in humans.
At the cellular and molecular levels, insulin’s actions indeed coordinately enhance the synthesis of triacylglycerol, the central currency of stored lipid in humans.
Insulin signalling enhances lipid storage in adipocytes by both stimulating triacylglycerol synthesis and inhibiting its breakdown.
Insulin’s potent inhibition of lipolysis not only favours lipid storage but also markedly decreases circulating fatty acid levels.
insulin action to inhibit lipolysis in this multifaceted mode provides a powerful restraint on the release of fatty acids from triacylglycerol within adipocyte lipid droplets.
Two pathways stimulated by insulin contribute to the pool of fatty acids that is esterified into triacylglycerol in adipocytes: fatty acid uptake from circulating triacylglycerol and de novo fatty acid synthesis.
Fat mobilization is strongly inhibited by insulin
Insulin is the major hormone encouraging lipolysis of circulating TAG-rich lipoproteins, while also suppressing the release of NEFAs from adipose tissue and promoting re-esterification of NEFAs within adipocytes