Insulinic regulation of the adipose tissue metabolism

Just a few quotes from scientific articles. I found them suggestive.

«Metabolic actions of insulin in men and women»

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

«Fatty Acids, Obesity, and Insulin Resistance: Time for a Reevaluation»

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

«Tracing the fate of dietary fatty acids: metabolic studies of postprandial lipaemia in human subjects»

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.

«Regulation of Lipogenesis by Glucocorticoids and Insulin in Human Adipose Tissue»

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.

«Dietary fat modifies lipid metabolism in the adipose tissue of metabolic syndrome patients»

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

«Regulation of Lipolysis in Adipocytes»

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.

«Advances in adipose tissue metabolism»

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 mechanisms for triacylglycerol storage»

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.

«The role of adipose tissue dysfunction in the pathogenesis of obesity-related insulin resistance»

Fat mobilization is strongly inhibited by insulin

«Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome»

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

Further reading:

  1. laura haydee alviani genoves

    Disculpa, me podrías dar el enlace en español? Gracias‼

    Enviado desde mi Windows Phone ________________________________

  2. Vicente

    «Relationship of Insulin Dynamics to Body Composition and Resting Energy Expenditure Following Weight Loss»

    As an anabolic hormone, insulin mediates postprandial conversion of glucose and lipids into storage forms (12). Increased insulin action promotes body fat gain (13), as demonstrated by chronic insulin administration in animals (14), initiation of insulin treatment in type 2 diabetes (15), and excessive insulin treatment in type 1 diabetes (16)—an effect that appears to be at least partially independent of energy intake (17). Moreover, high endogenous insulin secretion arising from genetic variation (18), pancreatic tumor, hypothalamic damage, or other causes (19) is prospectively associated with weight gain, whereas drugs
    that inhibit insulin secretion attenuate weight gain (20). Indeed, among patients with type 2 diabetes receiving standard treatment, high insulin action may adversely affect energy expenditure (21).

  3. Vicente

    In order to accumulate body fat, you need a few things in place. First thing you need, is access to ad lib calories. Obesity cannot occur during food restriction. Second thing you need, is the genetic potential for your fat cells to rapidly, and powerfully, respond to insulin with fat gain. Third thing you will need is excessive insulin production.
    If either of these conditions are not met, obesity is physically impossible.

    «Response to: Does High Circulating Insulin Drive Body Fat Accumulation?«

  4. Vicente

    Lipogenesis is highly influenced by factors such as feeding, fasting, and diet composition. Excessive carbohydrate consumption stimulates lipogenesis in both the liver and AT, increasing the availability of TAG in the postabsorptive state. In contrast, a high-fat/low-carbohydrate diet and fasting reducesde novo lipogenesis and lipogenesis, respectively, in AT (12). These changes are related to the increased or reduced expression and activity of LPL enzyme (high-carbohydrate/high-fat diets and fasting, respectively). In addition, it has been reported that the reduced lipogenic response during fasting is primarily due to a decreased capacity of white AT to generate acetyl-CoA from glucose, rather than an inhibition of lipogenic enzymes involved in FA synthesis.

    Blood glucose levels act directly on lipogenic capability via three distinct mechanisms. First, because glucose is a substrate for lipogenesis, thus producing acetyl-CoA by glycolysis, glucose activates FA synthesis (13). Second, glucose stimulates the lipogenic enzyme synthesis of ATP-citrate lyase, G6PDH, ACC, malic enzyme, and FAS (8). Finally, glucose promotes lipogenesis by stimulating insulin secretion and inhibiting glucagon release from the pancreas (6).(source)

Deja un comentario. Si los comentarios no contribuyen/aportan a los artículos publicados no los publico. Tampoco los publico si intentan forzar un debate o una toma de postura que el autor no ha planteado o que ha dado por cerrada. No publico comentarios descalificativos ni críticas fuera de lugar o que considere que no aportan nada. Si percibo intención de molestar en lugar de participar, o si no detecto vida inteligente, tampoco será publicado.

Introduce tus datos o haz clic en un icono para iniciar sesión:

Logo de

Estás comentando usando tu cuenta de Salir /  Cambiar )

Imagen de Twitter

Estás comentando usando tu cuenta de Twitter. Salir /  Cambiar )

Foto de Facebook

Estás comentando usando tu cuenta de Facebook. Salir /  Cambiar )

Conectando a %s

Este sitio usa Akismet para reducir el spam. Aprende cómo se procesan los datos de tus comentarios.