К ВОПРОСУ О НЕКОТОРЫХ КОРРЕЛЯЦИОННЫХ ВЗАИМОСВЯЗЯХ МЕТАБОЛИЧЕСКОГО СИНДРОМА И НЕАЛКОГОЛЬНОЙ ЖИРОВОЙ БОЛЕЗНИ ПЕЧЕНИ | Опубликовать статью РИНЦ

К ВОПРОСУ О НЕКОТОРЫХ КОРРЕЛЯЦИОННЫХ ВЗАИМОСВЯЗЯХ МЕТАБОЛИЧЕСКОГО СИНДРОМА И НЕАЛКОГОЛЬНОЙ ЖИРОВОЙ БОЛЕЗНИ ПЕЧЕНИ

Научная статья

Мосина Л.М.¹, Коробков Д.М.^2, *, Степанов Н.Ю.³, Титойкина Ю.В.⁴, Куманяева Д.Ю.⁵, Рахматуллина М. А.⁶, Сургаева Е. И.⁷, Мокина Е. А.⁸

¹ ORCID: 0000-0001-6831-3116;

² ORCID: 0000-0001-8948-0052;

³ ORCID: 0000-0002-8293-9753;

⁴ ORCID: 0000-0001-9974-359X;

^{1, 2, 3, 4, 5, 6, 7, 8} Национальный исследовательский Мордовский государственный университет им. Н. П. Огарева, Саранск, Россия

* Корреспондирующий автор (doctordmk[at]mail.ru)

Аннотация

Данный обзор литературы посвящен корреляционным взаимосвязям метаболического синдрома и неалкогольной жировой болезни печени (НЖБП). Сегодня мировая практика исследований требует всестороннего подхода к изучению заболеваний, что обусловлено мультифакторным подходом. Пожалуй, наиболее значимыми в формировании НЖБП являются: сахарный диабет 2 типа, инсулинорезистентность, ожирение, так как они в свою очередь выступают самыми значимыми компонентами метаболического синдрома. Но по–прежнему дискутабельным вопросом являются стеатозные изменения в печени, которые могут выступить в качестве инициирующе компонента метаболического синдрома.

Ключевые слова: метаболический синдром, неалкогольная жировая болезнь печени.

ON THE QUESTION OF SOME CORRELATION LINKS OF THE METABOLIC SYNDROME AND NONALCOHOLIC FATIAL LIVER DISEASE

Research article

Mosina L.M.¹, Korobkov D.M.^2, *, Stepanov N.Yu.³, Titojkina Yu.V.⁴, Kumanyaeva D.Yu.⁵, Rahmatullina M. A.⁶, Surgaeva E. I.⁷, Mokina E. A.⁸

¹ ORCID: 0000-0001-6831-3116;

² ORCID: 0000-0001-8948-0052;

³ ORCID: 0000-0002-8293-9753;

 ⁴ ORCID: 0000-0001-9974-359X;

^{1, 2, 3, 4, 5, 6, 7, 8} National Research Mordovia State University, Saransk, Russia

* Corresponding author (doctordmk[at]mail.ru)

Abstract

This review of the literature is devoted to the correlation relationships of metabolic syndrome and non-alcoholic fatty liver disease (NAFTLD). Today, the world practice of research requires a comprehensive approach to the study of diseases, due to the multifactorial approach. Perhaps the most significant in the formation of NBBP are: insulin resistance, type 2 diabetes, dyslipidemia, obesity, and they, in turn, are the most important components of the metabolic syndrome. But still a debatable issue are steatal changes in the liver, which can act as an initiating component of the metabolic syndrome.

Keywords: metabolic syndrome, non-alcoholic fatty liver disease.

There is a view that non-alcoholic fatty liver disease (NAFTLD) is a manifestation of the metabolic syndrome (MS) [1, P. 2062], [10, P. 664]. Interest in NAFTLD is due to the prevalence of this disease among the population. NAFTLD is one of the most extensive forms of liver disease in all countries. According to world statistics, the prevalence of NAFTLD is 20-30% [2, P. 390].  In the Russian Federation, the results of an open randomized prospective study observation of DIREG_L_01903 NAFTLD were found in 26,1% of patients, among whom liver cirrhosis was detected in 3%, steatosis – in 79,9%, steatohepatitis – in 17,1% [3, P. 335], [11, P. 303]. More often, NAFTLD is detected in patients with diabetes mellitus (up to 63%) and obesity (up to 93%). The risk of NAFTLD disease is equal in people of different ages and nationalities [2, Р. 393].

Many NAFTLD researchers see IT as an integral part of the MS. The frequency of occurrence of NAFTLD varies from 14 to 26%, in addition, 10% of patients show signs non-alcoholic steatohepatitis [4, P. 92], [6, P. 7238].

It used to be considered that NAFTLD is easy, but then it turned out that NAFTLD leads to cirrhosis in 4-30% of cases, and steatohepatitis leads to fibrosis, and then to liver necrosis.

Since 2003, following the results of the 1st World Congress on IR, held in the USA, it has been decided that NAFTLD, along with hypertension and type 2 DM, is part of МS [5, P. 18].

F. Angelico et al. In 2015, 308 patients with MS were examined, and NAFTLD was found in 95,5% of patients, with a positive correlation between steatosis and MS clinical manifestations [12, Р. 325].

Severe forms of steatosis are usually associated with the presence of 5 clinical and biochemical signs of MS according to ATP III criteria. The first research in this direction was conducted by Marchesini et al. (2016), 304 patients with NAFTLD were examined for signs of metabolic syndrome in 88% of cases [9, P. 475].

Japanese doctors examined 4401 people with a normostenic body constitution, in which NAFTLD was clinically confirmed only in 18%, after one year NAFTLD was detected in 10% of patients, which the authors associate with MS [8, P. 12].

NAFTLD is a manifestation of MS, and its pathogenesis is based on insulin resistance (IR), even in 2013, a study was conducted, according to the results of which M. Rashid and E. Roberts suggested that IR is the cause of fat accumulation in [6, Р. 7238]. Proponents of this theory claim that liver steatosis is the result of an increase in the accumulation of free fatty acids in the IR. The association of NAFTLD with MS manifestations, especially in the most severe stages of liver disease, confirms the reason for the role of IR [6, Р. 7239]. A number of authors believe that the additional deposition of fat in the liver reduces the sensitivity of hepatocytes to insulin, which leads to resistance to hepatic insulin. T. Wannan et al. (2016) NAFTLD and hepatic IR without peripheral IR were detected in an experiment in rats after 3 days of feeding with a high percentage of fat. Prevention of fatty liver leads to increased insulin sensitivity [9, Р. 475]. Similar results were also obtained by Boden et al. (2007) and L.Ryssy (2015). The degree of IR was proportional to the concentration of free fatty acids in the liver.

L. Ryyssy et al. (2015) observed that NAFTLD in patients with type 2 DM determined the amount of insulin needed to correct hyperglycemia.

Other authors share the opinion that the accumulation of free fatty acids can occur without the development of peripheral IR, but the hepatic IR develops.

Steatosis is a secondary condition to IR and dyslipidemia, which complicates its therapy. Interesting results were obtained in the study of David et al. (2016) in which 63% of patients with obesity and type 2 diabetes had NAFTLD. At the same time, the authors note that among these patients, the detected IR is significantly higher than among patients with type 2 diabetes without the development of NAFTLD. These data are consistent with the opinion оf M. Giloter (2015) [12, P. 325].

NAFTLD is closely associated with obesity. The survey S. Bellentani (2016), of 66 obese people revealed the presence of NAFTLD in 87,5%. The study Varceau P. et al. of 555 patients with obesity grade 3: 86% had steatosis, 24% – steatohepatitis, 75% – fibrosis, 2 % – liver cirrhosis. According to A. O. Bauerova et al. (2005) obesity is associated with the development of steatosis in 95% of cases and with the development of NAFTLD in 20-47%. In 75% of patients with NAFTLD the body mass index increased by 10-42% in comparison with the norm and Stepanov steatosis is directly proportional to the degree of obesity. According to other data, the prevalence of obesity in people with NAFTLD varies from 30 to 100%.

According to T. Gottoet al. (2014) NAFTLD is associated with abdominal obesity. The Central localization of fat is detected in patients with NAFTLD, not obese [7, P. 360]. This is explained by the fact that in the case of excess portal or intraperitoneal fat can increase the flow of free fatty acids through the portal vein to the liver with the development of steatosis.

On the contrary, there is an alternative view that the greater impact on the formation of the NAFTLD has an excess of extraperitoneal fat mass.

1. Steppala-Lindroos et al. (2016) in their study showed that fat accumulation in the liver develops independently of intra – or extraabdominal fat distribution. Several studies have generally not revealed the relationship between the development NAFTLD and abdominal obesity [4, P. 91].

The view that diabetes type 2 develops NAFTLD shared by many authors. A number of studies have revealed the development of NAFTLD in 75% of patients with type 2 diabetes. In turn, type 2 diabetes mellitus and increased blood glucose levels were noted in 34-75% of patients with NAFTLD. Other authors point to the high prevalence of carbohydrate metabolism disorders in patients with NAFTLD. H. Knkobler et al. (2009) a study of 48 cases of NAFTLD revealed type 2 DM in 44%. In a similar study conducted by Younossi Z. et al. (2014) type 2 DM is detected in 33% of patients, with the severity of NAFTLD was higher in patients with type 2 DM [10, P. 667], [11, P. 308].

There is now strong evidence that NAFTLD often precedes the development of DM 2. NAFTLD is simply «hepatic manifestation» MS is out of date. NAFTLD is an important factor in the onset of diabetes and an early sign of diabetes and other clinical manifestations of MS.

Communication NAFTLD with hyperlipidemia has been noted by many researchers. It is well known that NAFTLD with hypercholesterols is more common. Along with this, the majority of patients with NAFTLD revealed a decrease in blood cholesterol Low density lipoprotein. According to D. Nievelis et al. (2017), liver steatosis may affect the severity of dyslipidemia in type 2 DM.

There are some studies showing the relationship of NAFTLD with hypertension. For example, in the study of J. Dixon et al. (2014) with 105 patients with NAFTLD, high IR index and hypertension were independent risk indicators for the development of NAFTLD [10, P. 667]. The connection of NAFTLD with IHD also emphasizes the common mechanisms of development of the above diseases in MS, in addition, NAFTLD is often combined with gallbladder dyskinesia.

Thus, it follows from the literature review that, despite the abundance of works, there are many contradictions that require further research in this area.

Конфликт интересов Не указан.

Conflict of Interest None declared.