Журнал «Здоровье ребенка» 6 (49) 2013

Now scientists pay a close attention to a role of metabolic factors in arterial hypertension (AH) formation, and especially to the hormones produced by adipose tissue and hormone-active peptide [3, 4 12, 14].  For the last decade the phenomenon of insulin resistance

 [3, 7, 13] have been becoming the leading mechanism of formation of AH and a some cardiovascular risk factors.  For the last years many authors have been interesting by  leptin and ghrelin. However their value in a children's organism and their communication with IR, carbohydrate and lipide exchanges at AG remains unlit in literature especially in case of a combination of AG with an obesity and excess mass of a body.  Therefore research of metabolic factors at AG is actual and perspective in respect of prophylaxis of a progressing course of a disease.

The purpose of our work was studying of some indicators of carbohydrate metabolism, and also leptin's and ghrelin's levels at children with the primary arterial hypertension (PAH).

Materials and methods

We have examined 164 children at the age of 12-17 years with PAH. We have chosen 2 ways of researches. In the first way children were divided into 2 groups depending on the AH form. There were group of children with  stable AH (SAH) and group of children with labile AH (LAH). In the second case of group were formed depending on the index of weight of a body (IWB). As a result 2 groups of children with normal IMT (IMT lower than 25) and with raised IMT (IMT higher than 25) turned out. The group of control (KG) was made by 30 healthy children with a normotension and the normal IMT,wich were comparable to the main group on age and a sex.

All children were investigated on a metabolic profile which included definition of fasting level in blood and level of glucose after sugar loading by the standard glucose tolerance test, and also insulin levels,leptin and ghrelin in blood serums by the immunofermental methods. Assessment of an insulin resistance carried out by means of the computer HOMA 2 model and the HOMA_R and Caro indexes. As a result we established hyperinsulinemia and IR existence by HOMA_R at 103 (62,8 %) children and 108 (65,9%) children respectively at the average level of glucose 4,27±0,05 the mmol/l being in limits of normal reference values. However IR was revealed at 152 (92,7 %) patients by means of the computer HOMA 2  model. And this syndrome was hidden at 49 (26,8%) from patients with IR,  since wasn't defined by other techniques.

A concentration of glucose after sugar loading was in limits of normal values, however it was authentically above, than in group of control (P<0,001) at all teenagers.

The analysis of insulin concentration have been showed that in group with LAH the children prevailed who had normal and boundary insulin levels – 52 (46,0%) and 36 (31,9%) children respectively, unlike patients with SAH, at which the high and boundary hyperinsulinemiya have been met more often, so at 27 (52,9%) and at 15  (29,4 %) people respectively. Also the hyperinsulinemiya have been progressed authentically during the weighting of a disease and increase of a body mass indeх.

In the analysis of an insulin exchange the IR has been  found and it has been confirmed by the increased insulin secretion by β–cells (B %) and a low insulin sensitivity of the tissues (S%) at patients with the LAH and SAH in сontrast to healthy. However, at teenagers with SAH average values of S % were authentically below (P<0,001), and IRI HOMA 2 was reliable above unlike children with the labile form (P < 0,001) at tended to indicator increase B % with weighting of a disease and BMI increase. It can testify to the bad forecast of a disease and further progressing of a syndrome of IR at PAH. Also average values of HOMA_R and Caro confirmed IR existence at both forms of AH and differed authentically from KG (P < 0,001). However children with SAH and BMI > 25 had authentically above values of the HOMA_R index and reliable below the Caro index, unlike children with the LAH and normal BMI.

In the analysis of leptin and leptin resistance (LR) it was noticed that boys and girls have been had a hyperleptinemiya and a leptin resistance which was more expressed at children with SAH. LR existence possibly specifies that sensitivity of the hypothalamic centers to лептину – to a hormone of saturation decreases and its ability in appetite regulation with weighting of AH  that can promote  to obesity development against AG and to the adverse course of a disease is lost over time. At the same time such hyperleptinemiya plays a role of the compensatory mechanism as leptin slows down effect of insulin on gluconeogenesis in a liver, strengthening activity phosphate enolum pyruvate carboxykinase, inhibiting thyrosinum phosphorylation – substrate of an insulinic receptor in a muscular tissue and stimulated insulin glucose transport in fatty tissue [11].

Also the found decreased ghrelinemiya at children with AG, more expressed at SAH is point out the disturbance of a regulation of appetite at AH . Also low ghrelin levels existence has been established at 66 (40,2%) children with an obesity and AH at which the regulation of appetite is unambiguously broken.    It only confirms that regulatory mechanisms of leptin-ghrelin interactions are lost at children with AG .  

Also a hypoghrelinemiya, a hyperleptinemiya and LR at boys and the girls, more expressed at children with BMI > 25 have been observed. However a  gender differences in leptin and ghrelin levels have been leveled  at excess of body mass. On our mind it can be related to disturbance in a metabolism of sexual hormones and a hypersecretion of estrogens at excess of a body mass at boys. And the hyperleptinemiya and hypoghrelinemiya combination at children a lot of a body mass confirms opinion of other researches on the broken regulation of appetite by these hormones at an obesity.

Conclusions

1.The hyperinsulinemiya, a hyperleptinemiya, a leptin resistance and a hypoghrelinemiya in the conditions of an insulin resistance at normal physiological level of a glucose at children with primary arterial hypertension, more expressed in groups with stable arterial hypertension and with excess mass of a body.

2.It is established that leptin-ghrelin mechanisms of a regulation of appetite are lost at children with primary arterial hypertension  regardless of body mass.

3.The insulin resistance is a leading pathogenetic link in development of other metabolic disturbances at children with primary arterial hypertension.