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Endocrine Implications of Obesity and Bariatric Surgery Praca Poglądowa/review Endokrynologia Polska DOI: 10.5603/EP.2018.0059 Tom/Volume 69; Numer/Number 5/2018 ISSN 0423–104X Endocrine implications of obesity and bariatric surgery Michał Dyaczyński1, Colin Guy Scanes2, Helena Koziec3, Krystyna Pierzchała-Koziec4 1Siemianowice Śląskie Municipal Hospital, Department of General Surgery, Siemianowice Śląskie, Poland 2Centre in Excellence in Poultry Science, University of Arkansas, Fayetteville, Fayetteville, Arkansas, USA 3Josef Babinski Clinical Hospital in Krakow, Poland 4Department of Animal Physiology and Endocrinology, University of Agriculture in Krakow, Poland Abstract Obesity is a highly prevalent disease in the world associated with the disorders of endocrine system. Recently, it may be concluded that the only effective treatment of obesity remains bariatric surgery. The aim of the review was to compare the concepts of appetite hormonal regulation, reasons of obesity development and bariatric pro- cedures published over the last decade. The reviewed publications had been chosen on the base on: 1. reasons and endocrine consequences of obesity; 2. development of surgery methods from the first bariatric to present and future less aggressive procedures; 3. impact of surgery on the endocrine status of patient. The most serious endocrine disturbances during obesity are dysfunctions of hypothalamic circuits responsible for appetite regulation, insulin resistance, changes in hormones activity and abnormal activity of adipocytes hormones. The currently recommended bariatric surgeries are Roux-en-Y gastric bypass, sleeve gastrectomy and adjustable gastric banding. Bariatric surgical procedures, particularly com- bination of restrictive and malabsorptive, decrease the body weight and eliminate several but not all components of metabolic syndrome. Conclusions: 1. Hunger and satiety are mediated by an interplay of nervous and endocrine signals. 2. Healthy adipose tissue secretion of adipokines is coordinated in an anti-inflammatory, insulin-sensitizing and cardioprotective pat- tern. However, with increasing fat mass this secretion pattern is changed into a proinflammatory, insulin resistant, atherogenic and fatal systemic environment . 3. Bariatric surgery is not a solution of the obesity problem for everyone. 4. Long term postsurgical observations of the hormonal profile changes are necessary and should be obligatory. (Endokrynol Pol 2018; 69 (5): 574–586) Key words: obesity, endocrine dysfunctions, bariatric surgery, gastrointestinal hormones Introduction For this reason World Health Organisation (WHO) of- ficially declared obesity as a global epidemic in 1997 [4–6]. Obesity is a highly prevalent disease in the world, and The causative treatment of obesity is still fragmen- it is caused by an excess of nutrients, genetic back- tary because of the large inter-individual variability and ground, lack of physical exercise, or a disorder of the absence of pre-treatment data, making interpretation of hypothalamo-gastrointestinal axis activity. Adiposity the results difficult. For this reason, treatment with con- excessive signals such as leptin and insulin as well as servative symptomatic methods, e.g. dietetic, pharma- gastrointestinal hormones affect the metabolism of fat, cological, or behavioural, are usually doomed to failure carbohydrates and destroy the balance between energy and never achieve the required results [7]. The efficacy spending and consumption [1, 2]. of these methods in long-term weight loss without Hunger and satiety are mediated by an interplay of a yo-yo effect is estimated to be as little as 5% [8]. Some nervous and endocrine signals. Neural signalling takes of the other methods (e.g. jaw-wiring), although effec- place between the hypothalamus and other parts of the tively promoting weight loss, for humanitarian reasons central nervous system to regulate food intake accord- cannot be used [9]. Recently, it may be concluded that ing to caloric need [3]. the only effective treatment of obesity remains surgery. Morbid obesity was considered as a disease from the However, it must be pointed out that bariatric surgery, second half of the 20th century. In highly developed coun- in spite of food intake suppression, has a strong effect tries morbid obesity shows an extremely fast-growing on the metabolism, particularly carbohydrate and lipid tendency; it was found that since 1980 its rate doubled. turnover, as well as on the hormonal system [10]. Krystyna Pierzchała-Koziec, Katedra Fizjologii i Endokrynologii Zwierząt, Uniwersytet Rolniczy w Krakowie, Al. Mickiewicza 24/28, 30–059 Kraków; tel.: 698 630 422, faks:12 633 33 07, e-mail: [email protected] 574 Endokrynologia Polska 2018; 69 (5) A B Effect Food intake Energy expenditure Effect Food intake Energy expenditure PVN MC4R NPYR PVN MC4R NPYR MSH MSH NPY NPY ARC GABA ARC GABA AgRP AgRP POMC POMC Leptin Peripheral signals Peripheral signals Ghrelin Serotonin Figure 1. Hypothalamic circuits of appetite and satiety. A. Anorexigenic pathway. B. Orexigenic pathway AgRP — agouti-related peptide; ARC — arcuate hypothalamic nucleus; GABA — gamma-aminobutyric acid; aMSH — a-melanocyte- stimulating hormone; MC4R — a-melanocyte-stimulating receptor; NPY — peptide Y; NPYR — receptor of NPY; POMC — proopiomelanocortin; PVN — paraventricular nucleus Thus, based on different opinions on the effica- create two pathways — anorexigenic and orexigenic ciousness of morbid obesity treatments, the aim of the — which are responsible for food intake and energy present review was to compare the most important expenditure (Figure 1) [12]. changes in the concepts of food intake regulation, obe- sity development, and bariatric procedures (methods, Orexigenic pathway acceptance, popularity, and side effects) in recent years. The reviewed publications were chosen based on: Neuropeptide Y and agouti-related peptide (NPY/ 1. reasons and consequences of obesity, particularly /AgRP) neurons have axon terminals that release gam- hormonal changes; ma aminobutyric acid (GABA, an inhibitory neurotrans- 2. development of surgery methods from the first mitter) to suppress the proopiomelanocortin (POMC) bariatric to present and future less aggressive; and neurons and oxytocin neurons in the paraventricular 3. the ability to assess the effects of bariatric surgery nucleus of the hypothalamus (PVN). On the other hand, POGLĄDOWE PRACE on the endocrine status of the patient. PVN neurons expressing pituitary adenylate cyclase- activating polypeptide (PACAP) have axon terminals Regulation of food intake by that release glutamate (an excitatory neurotransmitter) hypothalamo-gastrointestinal axis to activate NPY/AgRP neurons [13]. The anorexigenic pathway is stimulated by peri- Historically, it was established that the anorexigenic pheral leptin receptors in the arcuate nucleus of the hy- centre (appetite suppressing) is located in the ventro- pothalamus (ARC). As an effect of that activity, secreted medial hypothalamus [11]. The orexigenic (appetite POMC stimulates melanocortin receptors in the PVN stimulating) centre is in the area of the lateral hypo- (inhibition of food intake) and IML (intermediolateral thalamus. The hypothalamus receives the signals from region of the spinal cord), responsible for increasing the periphery derived by nervous route — predomi- energy expenditure [14–16]. nantly the vagus nerve, and endocrine route — mainly Recently, a hypothesis has been proposed stating by ghrelin, leptin, and insulin secreted into the blood. that feeding is regulated by special neurons inside The reaction of the hypothalamus to these signals is specific hypothalamic nuclei, and not by centres in the characterised by changing activity of two opposite brain. According to many publications, there are three circuits — stimulation or inhibition of food intake. The main ways of signalling from the periphery responsible hypothalamic circuits of hunger/appetite and satiety for information about hunger or satiety: 575 Hormones, obesity and bariatric surgery Michał Dyaczyński et al. 1. short-term effects on food intake from gastrointes- Table I. Gastrointestinal hormones and pancreatic hormones tinal hormones (orexigenic or anorexigenic) [16]; involved in appetite regulation 2. direct mechanical stimulation of the gastrointestinal tract, mainly stomach and duodenum [17]; Gastrointestinal hormones 3. Long-term effects on food intake provided by adi- Place of Effects pose tissue hormones [18]. synthesis Development of different methods — genetic, op- Cholecystokinin Duodenum Pancreatic exocrine secretion togenetic, and molecular — together with established Gastrointestinal motility methodologies allow us to have a refined understand- Secretin Intestine Pancreatic exocrine secretion ing of neural circuits that regulate feeding behaviour. Motilin Intestine Gastrointestinal motility Gastrin Stomach Acid secretion Gastrointestinal hormones Peptide P Small intestine Gastrointestinal motility Gastrointestinal (GI) hormones are predominantly Galanin Small intestine Gastrointestinal motility polypeptides produced in and secreted from special- Insulin inhibitor ised gut endocrine cells. These peptides are involved Taste in GI motility, secretion, absorption, growth, and GLP-2 Small intestine Gastrointestinal motility development. Many of the peptides in the GI tract Growth are also found in the enteric nervous system and the Oxyntomodulin Small intestine Satiation central nervous system. Gastrointestinal (GI) peptides PYY Small intestine Satiation are classified into families
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