Forgot your password?

Registration

company

brands

An unpredictable error occurred on the server. It will be fixed soon

Did you notice an error? Contact the editor

A confirmation email has been sent to your {email} email!

Your password has been successfully changed!

Something went wrong. Please try again later.

The password change request has been successfully sent to your email address.

Rules for publishing comments

The article was translated into English using automatic translation. The editors are working on its improvement.

we are working on a translation. Follow the link or use Google Translate

<a href="https://www.instagram.com/cosmetology.pro.bhub/?hl=ru" style="font-size: 16px;" target="_blank"><img alt="" src="https://pro.bhub.com.ua/cosmetology/upload/files/%D0%A1%D0%90%D0%99%D0%A2/BANER_PROCosm-insta.gif" /></a><hr /> Elena Balym, dermatocosmetologist, member of the UADV, specialist in injection techniques, certified trainer of Mesopharm, Hinoki Clinical, Neoglis, Pressensa, Medicare (Ukraine)<hr /> Aesthetic medicine specialists are increasingly faced with procedures for the correction of local fat deposits both in the face and on the body. Often, patients demand that cosmetologists solve the problem as soon as possible and hope that the effect will last forever. In order to understand what results we can achieve, what determines how long the effect is maintained, it is necessary to understand the principles by which adipose tissue functions and what factors influence it .<blockquote> In addition, you need to understand for yourself and be able to explain to the patient that correction of local fat deposits and working with excess weight are related concepts, but not the same thing</blockquote> In both the first and second cases we are talking about working with adipose tissue. However, when correcting local fat deposits, we work with a small area of ​​adipose tissue and eliminate only a local defect, while when working with excess weight, global work is carried out, affecting a whole complex of complex relationships between different systems and tissues of the body. A thorough study of the functioning of the endocrine and digestive systems, metabolism, lifestyle and habits, and the psycho-emotional state of the patient is necessary. It is important to understand the complexity and methodical nature of the approach, both on the part of the specialist and on the part of the patient himself. Working with excess weight requires time, patience, perseverance and a balanced, competent approach, as well as a clear understanding of what adipose tissue is, what it consists of, and by what principles it works. At the moment, a sufficient amount of knowledge has been accumulated about its anatomical and physiological features and how its work can be controlled. What is adipose tissue So, adipose tissue is a type of connective tissue that consists of adipocytes (lipocytes) and their precursors (preadipocytes), fibroblasts, mast cells, macrophages, nerve cells and vascular wall cells. The bulk of adipose tissue is occupied by adipocytes, and they are the object of close study. What do we know about these cells? There are several varieties of them - brown, beige and white adipocytes. Brown adipocytes Brown adipocyte is the main cell of brown adipose tissue. It is 10 times smaller than a white lipocyte. The nucleus is located in the center of the cell (unlike a white lipocyte, it is not displaced to the periphery), mitochondria are highly developed, surrounding numerous fat droplets distributed throughout the cytoplasm. The oxidative capacity of mitochondria is 20 times higher than in white adipose tissue; mitochondrial cytochromes provide the characteristic brown color of the tissue. Mitochondria contain a special protein called thermogenin (UCP-1), which makes up 5% of the total protein in them. It uncouples oxidative phosphorylation and respiration, so energy is not stored in the form of ATP, but is used to quickly warm the body. There are two types of brown adipocytes: classic (derived from myoblasts) and transformed (recruited, beige, derived from white adipocytes). The latter can appear in white adipose tissue and muscle in adults. Obesity leads to decreased activity of brown adipocytes. Brown adipose tissue Brown adipose tissue is well developed in newborns (accounting for 2–6% of body weight), in an adult it is preserved in the neck, interscapular region, around the kidneys, aorta and in the mediastinum, and in other areas it is replaced by white adipose tissue. Women are twice as well developed as men; its quantity increases in the autumn-winter period. It is not yet known whether brown adipose tissue has its own endocrine function. The tissue is involved in thermoregulation and warming of the entire body or the organs that it surrounds (in young children); it is the central tissue that provides non-contractile thermogenesis, due to which the level of heat production can be increased three times compared to the level of basal metabolism. White adipocytes A white adipocyte is a large cell that has one large fat vesicle that occupies the entire cell, surrounded by a ring of cytoplasm and pushing the nucleus to the periphery. May transform into brown adipocyte in response to cold or catecholamine stimulation. White adipose tissue White adipose tissue performs trophic function, is a fat depot, is capable of breaking down and synthesizing fat, is involved in thermoregulation (a large amount of energy is released during the breakdown of fat). Adipose tissue helps retain heat in the body due to its poor thermal conductivity, prevents trauma to underlying tissues, ensures good skin mobility, masks various bony protrusions, produces hormones and hormone-like compounds (adipocytes and other adipose tissue cells). Localization of adipose tissue Based on localization, visceral and dermal fat (subcutaneous fat) are distinguished. Visceral fat Visceral adipocytes include fat cells of the omentum, retroperitoneal fat and the anterior abdominal wall. The number of visceral fat cells remains constant after puberty (11–12 years), despite fluctuations in body weight. Visceral adipocytes do not have receptors for insulin, contain a large number of glucocorticosteroid receptors, have increased sensitivity of β-adrenergic receptors and reduced sensitivity of α2-adrenergic receptors (lipolysis under the influence of catecholamines - adrenaline and norepinephrine), and are characterized by higher activity of 17β-hydroxysteroid DG. When losing weight, the number of visceral adipocytes does not decrease. Dermal fat Dermal fat has no limit on the number of fat cells; their number can increase. There are many preadipocytes that can turn into adipocytes, which have receptors for insulin, are the source of the formation of hair follicles in the anagen phase, are activated during injury, trigger renewal of the fibroblast pool, produce bactericidal agents: cathelicidins (against St. aureus), synthesize more leptin and adiponectin , than visceral adipocytes, have higher aromatase activity. They undergo differentiation less actively than visceral adipocytes (less susceptible to the influence of PPRA-γ). The process of growth of adipose tissue Adipocytes go through several stages in their development: preadipocyte (lipoblast), maturing preadipocyte, mature adipocyte. Activated cells divide mitotically several times and then become immobile again. The differentiation processes are regulated by the transcription factors PPRA-γ and C/EBP alpha (CCAAT-enhancer-binding protein alpha), which are controlled by hormones and potentiate each other’s action. Adipocyte differentiation is activated by glucocorticoids, IGF-1, and factors that increase the amount of cAMP. Suppresses the maturation of Pref-1 fat cells.<blockquote> Existing adipocytes may increase in size, causing an increase in body volume. On average, a fat cell can become 30–40 times larger than it was initially</blockquote> Small fat cells are more metabolically active than large ones and are also involved in the uptake of fatty acids. If the process of fat accumulation does not stop, the body sends a signal to preadipocytes, and they degenerate, forming new “storage facilities” for fat reserves.<blockquote> In obesity, the number of adipocytes can reach 100–130 billion cells, while their normal number should not exceed 30–35 billion</blockquote> The synthesis of fats and the development of adipose tissue is under hormonal and nutritional control. Thus, α-adrenergic receptors of adipocytes are sensitive to insulin, estrogens, and prolactin. Activation of these receptors leads to increased lipogenesis (formation of triglycerides). In turn, β-adrenergic receptors are sensitive to the effects of glucagon, testosterone, growth hormone, and cortisone. When they are activated, adenylate cyclase activity increases and cAMP accumulates, which is a catalyst for adipocyte lipases. As a result, the processes of lipolysis are enhanced - the breakdown of adipocyte triglycerides into glycerol and fatty acids, which leads to a decrease in the vacuole and the size of the fat cell itself. Lipolysis and lipolytics If it is necessary to generally reduce the volume of adipose tissue, an integrated approach is needed - correction of the hormonal status of the body, diet, and physical activity. What can we use in cosmetology practice? There are a number of drugs that affect the processes of lipogenesis and lipolysis, as well as causing necrosis or apoptosis of adipocytes. Substances that stimulate the breakdown of triglycerides in adipocytes to fatty acids and glycerol, activating β-adrenergic receptors, include yohimbine, theophylline, caffeine, green tea . It is possible to activate lipolysis by blocking phosphodiesterase: the process of splitting triglycerides requires sufficient activity of hormone-sensitive lipase, the work of which depends on a sufficient amount of cAMP. The production of cAMP, in turn, depends on the work of adenylate cyclase. The enzyme phosphodiesterase blocks the formation of cAMP and inhibits lipolysis. That is, when phosphodiesterase is blocked, it becomes possible to activate lipolysis. Substances that inhibit this enzyme include caffeine, aminophylline, theobromine, theophylline . When triglycerides are broken down, the resulting fatty acids must be transported into the mitochondria to provide energy and prevent their further conversion to triglycerides. Such a transporter of fatty acids is carnitine . In addition, there are substances that block α-adrenergic receptors and thereby suppress lipogenesis - the process of deposition of new fat. These include yohimbine and buflomedin . All of the above components belong to the group of so-called indirect-acting lipolytics , that is, drugs that affect metabolic processes in adipocytes, but do not destroy the cells themselves. However, there are drugs that act more actively and radically - direct lipolytics . They either destroy the membranes of fat cells, causing their necrosis and inflammation in adipose tissue (sodium deoxycholate), or trigger the process of apoptosis of adipocytes (pro-oxidants). Substances that inhibit lipogenesis and induce apoptosis include genistein, conjugated linoleic acid, docosohexaenoic acid, quercetin, resveratrol, esculetin . Resveratrol, for example, inhibits lipogenesis and lipocyte differentiation, activates lipolysis, and increases resistance to weight gain. Its effectiveness increases significantly when combined with vitamin D, genistein and quercetin. It must be remembered that direct or indirect lipolysis is possible only after high-quality preliminary tissue drainage and stimulation of peripheral blood flow. Obtaining an effect is possible with a well-designed treatment protocol. It is very important to maintain the resulting effect. And this will largely depend both on the patient himself and on correctly conducted explanatory work on the part of an aesthetic medicine specialist. That is, the work must be carried out comprehensively and systematically. And then success is guaranteed. First published in <a href="https://afisha.bhub.com.ua/event/magazines/lne/les-nouvelles-esthetiques-2019-1-100grn" target="_blank">&quot;Les Nouvelles Esthétiques Ukraine&quot; No. 1 (113) 2019</a>

Injection lipolysis: what is important to know