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52ВЗАИМОЗАВИСИМОСТЬ ЛЕПТИНА, ИНСУЛИНОВЫХ ГОРМОНОВ И
ОЖИРЕНИЯ
Ахмедов Шавкатбек Вахобов Лутфулло Абдурахимов Абдухалим Нугманов Озодбек
Андижанский государственный медицинский институт
Андижан, Узбекистан
Статья посвящена жизненно важной проблеме 21го века - ожирению. Оно может привести к серьезным патологиям. Это можно объяснить резистенцией к инсулину и лептину. Диабет и ожирение являются двумя метаболическими заболеваниями, характеризующимися резистентностью к инсулину и слабым воспалением.
Ключевые слова: ожирение, инсулин, лептин, лептинорезистентность, инсулинорезистентность, метаболическая эндотоксемия.
LEPTIN VA INSULIN GORMONLARI HAMDA SEMIZLIKNING O'ZARO
BOG'LIQLIGI
Ushbu maqolada XXI asrning dolzarb mavzusi yuzasida so'z yuritilgan. Semizlik jiddiy kasalliklarni keltirib chiqaradi. Buni insulin va leptinga rezistentlik bilan tushuntirish mumkin. Diabet va semizlik insulin qarshiligi va past darajadagi yallig'lanish bilan tavsiflanadigan metabolik kasalliklardir.
Kalit so'zlar: semizlik, insulin, leptin, leptinga rezistentlik, insulinga rezistentlik, metabolik endotoksemiya.
INTERDEPENDENCE OF LEPTIN AND INSULINE HORMONES AND OBESITY
Abstract: this article is focused on one of the vital problems of the 21st century-obesity. It can lead to very serious pathologies. This can also be explained by insulin and leptin resistance. Diabetes and obesity are two metabolic diseases characterized by insulin resistance and a low-grade inflammation.
Key words: obesity, insulin, leptin, leptin resistance, insulin resistance, metabolic endotoxemia.
DOI: 10.24411/2181-0443/2020-10100
Leptin hormone. Known to science [1-4] what leptin action and the concept of 'leptin resistance' Leptin, a polypeptide hormone that is produced by adipocytes in proportion to their triglyceride content, links changes in body energy (fat) stores to adaptive responses in the central control of energy balance. According to research [5-7] by binding to and activating the long form of its receptor (LEPR-B) in the brain, leptin decreases food intake while increasing energy expenditure. Evolutionary considerations, together with a large body of experimental data, indicate that a major physiologic role of leptin is to respond to and defend against reductions of body fat (and thus leptin) that might impair survival and reproductive fitness. Apart from the notable exception that their body fat mass is markedly increased, the phenotypes of humans and rodents lacking leptin or LEPR-B mirror the physiological response to starvation (e.g. hunger, decreased metabolic rate, infertility, immune dysfunction, insulin resistance). Thus, leptin is required for energy stores to be sensed in the central nervous system (CNS) and is thus essential for
functions such as normal energy homeostasis and reproduction. Leptin replacement effectively reverses the altered physiology associated with low leptin states, including genetic leptin deficiency (e.g. Lepob/ob mice and the rare humans with loss of function mutations in the leptin gene), lipodystrophic syndromes (in which the lack of adipose tissue results in a corresponding diminution of circulating leptin [8,9]) and otherwise normal humans who have undergone weight reduction and whose circulating leptin is therefore decreased as a result of the diminished fat mass [10-12]. Moreover, exogenous leptin acutely decreases feeding and body weight in normal animals and is a powerful determinant of energy expenditure in fasted animals [5,13,14]. These observations establish leptin deficiency as a key regulator of metabolic and neuroendocrine responses to states that are characterized by negative energy balance and weight loss. Although leptin administration reduces food intake in normal animals, food intake ultimately returns toward normal during prolonged leptin administration, once body fat stores have been substantially depleted [5]. Moreover, treatment with leptin alone (even at very high doses) is ineffective as a means to decrease food intake and body weight in obese animals and humans, although congenital leptin-deficiency states represent an exception to this rule [15]. Indeed, the subset of overweight and obese human subjects who demonstrate the strongest catabolic response to leptin are those at the lower end of the obese body mass index (BMI) range and those with relatively low leptin levels for any given BMI or adiposity level [16,17]. Together with the aforementioned finding of elevated circulating leptin levels in obese subjects (commensurate with their adipose mass) [18,19], these observations have inspired the notion of 'leptin resistance' in common forms of obesity [2 0], analogous to the insulin resistance that contributes to type 2 diabetes and that often coexists with 'leptin resistance' in obese individuals. Indeed, similar cellular mechanisms might attenuate the action of both hormones, as detailed below.
Interdependence obesity and leptin resistance. In addition [21,22] obesity and the notion of 'selective' leptin resistance It has been proposed that the maintenance of reproductive function, energy expenditure, sympathetic outflow and other leptin-regulated processes in the setting of DIO indicates impaired leptin action in obesity, restricted to the control of feeding. Note that although the effect of genetic lesions that impair specific leptin-regulated pathways might produce selective leptin resistance, these represent a different case from that of DIO. Several lines of evidence argue against a meaningful selectivity in leptin resistance in DIO. First, a variety of data suggests that leptin acts on both energy expenditure and feeding via overlapping sites and mechanisms and the nature of a process that might interfere with feeding but not energy expenditure is thus unclear. Indeed, although the ARC represents a major site of cellular leptin resistance in DIO, ARC leptin action modulates energy expenditure, glucose homeostasis and other aspects of leptin action in addition to participating in food intake. In addition, endogenous leptin clearly plays a role in limiting appetite in DIO, as food intake rapidly restabilizes after the initial increase of feeding on highly palatable, energy-dense chow. Indeed, increasing the palatability of food promotes increased food intake despite the integrity of cellular leptin action, although food intake returns toward normal as adiposity increases (with the attendant increase of leptin levels and action. The decrease of feeding and body weight upon the reinstatement of a normal chow diet suggests that the initial increase of food intake and subsequent adiposity represents a predictable response to the hedonic characteristics of the novel diet, rather than a response to diminution of leptin action. Thus, the transient increase and subsequent return of energy intake toward baseline during DIO support a model in which elevated leptin levels in obesity contribute to the control of hunger as well as energy expenditure. Furthermore, the response of obese humans to weight loss (which causes responses such as increased hunger, cold intolerance, and decreased thyroid and sympathetic tone) is fundamentally intact, suggesting that the 'extra'
leptin in obese individuals exerts biologically relevant effects on parameters additional to those involved in the control of feeding. If it can be postulated that the effect of weight loss from the obese state is to increase hunger and that this reflects ongoing leptin resistance, the same must also be true for the other factors (diminished thyroid tone, cold intolerance and so on) that also accompany weight loss. Thus, a variety of data argues against a meaningful selectivity (i.e. control of feeding only) in the attenuation of leptin action in DIO and common human obesity [21,22].
Interdependence of insuline hormone and obesity. According to a study by Chinese scientists [23] obesity can augment insulin resistance (IR), leading to increased risk of diabetes and heart disease. Leptin, ghrelin, and various fatty acids present in the cell membrane may modulate IR. One group sciencists in this study aimed to investigate the impact of weight loss on IR, serum leptin/ghrelin levels, and erythrocyte fatty acids, and studied the associations between changes in these variables. A total of 35 obese (body mass index > 2 7) adults participated in a weight loss program for 3 months. IR was assessed using homeostasis model assessment for insulin resistance (HOMA-IR). The obese participants had a mean weight loss of 5.6 ± 3.8 kg followed by a 16.7% and 23.3% reduction in HOMA-IR and leptin (p < 0.001) levels, and an 11.3% increase in ghrelin levels (p = 0.005). The level of erythrocyte saturates decreased by 2.8%, while the level of n-3 polyunsaturates increased by 16.8% (all p < 0.05). The changes in leptin levels (-5.63 vs. -1.57 ng/mL) were significantly different (p = 0.004) in those with improved IR (changes in HOMA-IR < 0) than those without improvement (changes in HOMA-IR > 0), though there were no differences in the changes of ghrelin (p = 0.120) and erythrocyte fatty acids (all p > 0.05) levels. After adjusting for age, gender, changes in ghrelin, and body fat, they found a significant correlation between decreases in leptin and less risk of no improvement in HOMA-IR levels [odds ratio (OR) = 0.69, p = 0.039]. In conclusion, a moderate weight reduction in obese participants over a short period significantly improved IR. This weight reduction concomitantly decreased serum leptin, increased ghrelin, and elevated some erythrocyte unsaturates. Only leptin correlated independently with IR improvement upon multivariable logistic regression analysis, which indicates that leptin may play a role in the modulation of IR following weight loss.
Conclusion: The article expressed hormonal changes in obesity and obesity. Mechanisms of action of leptin and insulin hormones and there is an organic link between insulin resistance and leptin resistance and obesity. A number of scientific studies have been conducted and proven to this effect. Obesity can lead to very serious pathologies. This can also be explained by insulin and leptin resistance.
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