ometendoОжирение и метаболизмObesity and metabolism2071-87132306-5524Endocrinology Research Centre10.14341/omet2014124-31ometendo-6656Research ArticleСтатьиArticlesПоказатели углеводного обмена и продукция инкретинов у больных морбидным ожирением, в том числе перенесших билиопанкреатическое шунтированиеGlucose metabolism and incretins level in morbidly obese patients and in patients after biliopancreatic diversion performed for morbid obesityDedovI I

академик РАН и РАМН, директор ФГБУ «Эндокринологический научный центр» Минздрава России; ФГБУ Эндокринологический научный центр Минздрава РФ

-MelnichenkoG A

член-корр. РАМН, директор института Клинической эндокринологии; ФГБУ Эндокринологический научный центр Минздрава РФ

melnich@endocrincentr.ruTroshinaE A

д.м.н., профессор, зав. отделением терапии с группой ожирения; ФГБУ Эндокринологический научный центр Минздрава РФ

troshina@inbox.ruMazurinaN V

к.м.н., ведущий научный сотрудник отделения терапии с группой ожирения; ФГБУ Эндокринологический научный центр Минздрава РФ

natalyamazurina@mail.ruOgnevaN A

аспирант отделения терапии с группой ожирения; ФГБУ Эндокринологический научный центр Минздрава РФ

OgnevaNA@yandex.ruYashkovY I

д.м.н., проф., врач-хирург; ЗАО «Центр эндохирургии и литотрипсии»

ya@yashkov.ruIlinA V

заведующий лабораторией клинической биохимии; ФГБУ Эндокринологический научный центр Минздрава РФ

alexilin2005@yandex.ru201415032014111№1 (2014)2431Copyright © Dedov I.I., Melnichenko G.A., Troshina E.A., Mazurina N.V., Ogneva N.A., Yashkov Y.I., Ilin A.V., 20142014Dedov I.I., Melnichenko G.A., Troshina E.A., Mazurina N.V., Ogneva N.A., Yashkov Y.I., Ilin A.V.Dedov I.I., Melnichenko G.A., Troshina E.A., Mazurina N.V., Ogneva N.A., Yashkov Y.I., Ilin A.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.omet-endojournals.ru/jour/article/view/6656

Проведено исследование показателей углеводного обмена при морбидном ожирении (МО), в том числе после бариатрических вмешательств. Первую группу составили пациенты с ИМТ > 40кг/м2 (n=22); 2-ю группу - пациенты, перенесшие билиопанкреатическое шунтирование (БПШ) (n=23); 3-ю (контрольную) группу - здоровые добровольцы, не имеющие ожирения и избыточной массы тела (n=22). Во всех группах проведен оральный глюкозотолерантный тест (ОГТТ) с 75 г глюкозы с исследованием уровней глюкозы, иммунореактивного инсулина (ИРИ), глюкагоноподобного пептида 1 типа (ГПП-1), глюкозозависимого инсулинотропного полипептида (ГИП) и глюкагона исходно и через 30, 60 и 120 минут. Больные МО имели самые высокие уровни глюкозы натощак, при этом у 68,2% обследованных (15 человек) были выявлены нарушения углеводного обмена (нарушенная гликемия натощак (НГН) у 4 чел. и нарушенная толерантность к глюкозе (НТГ) у 11 чел.). В группе БПШ отмечена тенденция к более низким постпрандиальным значениям уровня глюкозы, причем у 4 человек (17,4%) были зафиксированы гипогликемии (менее 2,8 ммоль/л). В группе МО уровень ИРИ натощак и значение индекса HOMA были самыми высокими (р<0,001). Во 2-й и 3-й группах пик концентрации ИРИ определялся на 30-й минуте ОГТТ и был выше в группе оперированных больных (р=0,026). В группе МО наибольшие значения ИРИ определялись на 60-й минуте и к моменту завершения теста не возвращались к исходному уровню. У больных МО отмечалось снижение базального уровня ГПП-1, а также отсутствие пикового повышения ГПП-1 в ответ на пероральный прием глюкозы. Базальные и пиковые уровни ГПП-1 были достоверно выше после БПШ (р=0,037 и р=0,022). В группе МО значения ГИП во всех исследуемых точках превосходили соответствующие значения, полученные в двух других группах. Базальная концентрация глюкагона не различалась в хирургической и контрольных группах, в то время как лица с МО имели исходно более высокие уровни глюкагона (p=0,013) и не отмечалось его подавление в ходе ОГТТ (p=0,076). Таким образом, у больных МО чаще выявляются инсулинорезистентность и пограничные нарушения углеводного обмена. Нарушение регуляции углеводного обмена при МО характеризуется гиперглюкагонемией, повышением уровня ГИП и снижением секреции ГПП-1. У пациентов, перенесших БПШ, секреция ИРИ и ГПП-1 в ответ на пероральный прием глюкозы значительно повышена, что обуславливает высокий риск постпрандиальных гипогликемий.

We’ve studied a carbohydrate metabolism in morbidly obese (MO) patients and the patients after bariatric surgery. The patients of the 1st group had BMI>40 (n=22) and no history of diabetes mellitus. Patients after biliopancreatic diversion (BPD) performed for MO were included in the 2nd group (n=23). The 3rd group was a control group of normal weight healthy subjects (n=22). Blood glucose levels, insulin, GLP-1, GIP and glucagon during the OGTT (with 75 g of glucose) at 0, 30, 60 and 120 minutes were measured in all patients. In MO group fasting glucose levels were the highest. Impaired glucose metabolism was revealed in 68.2% of patients (n=10). Impaired fasting glucose (IFG) was diagnosed in 4 cases (18.2%), impaired glucose tolerance (IGT) in 11 patients (50%). In the BPD postprandial blood glucose levels (120 min) were lower if compared to the other groups. In 4 individuals (17.4%) we found postprandial hypoglycemia (<2.8 mmol/l). Patients of the MO group had the highest fasting insulin levels and HOMA-IR (p<0.001). The maximum of insulin concentration was seen on minute 30 of the OGTT in the 2nd and 3rd groups, and it was significantly higher in the post-bariatric patients (p=0.026). In MO group the maximum of the plasma insulin levels were on the 60th minute and were still elevated after 120 minutes. Fasting and stimulated (on the 30th minute) levels of GLP-1 were significantly higher after BPD (р=0.037 and p=0.022 at 0 and 30 min, respectively). Morbidly obese patients had higher fasting and stimulated GIP. Fasting glucagon concentrations were similar in the surgical and control groups, while the people with MO had higher initial levels of glucagon (p=0.013) and it was not suppressed during the OGTT (p=0.076). Glucose intolerance and insulin resistance incidence was higher in MO patients. Hyperglucagonemia, increased GIP and decreased GLP-1 levels are observed in MO patients. Stimulated plasma insulin and GLP-1 concentrations were significantly increased in patients who underwent BPD, and may cause postprandial hypoglycemia.

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The authors declare that there are no conflicts of interest present.