Ghrelin: a new treatment for non-alcoholic fatty liver disease?

Delhanty, Patric J. D.; Lely, Aart Jan van der

doi:10.1007/s12020-012-9800-2

Cited by 5 publications

(2 citation statements)

References 11 publications

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“…Unacylated ghrelin is also present in circulating blood and the stomach, and the quantity is much greater than that of ghrelin (Kojima et al 1999, Hosoda et al 2000. Unacylated ghrelin exerts some biological actions, e.g., regulate feeding (Asakawa et al 2005, Toshinai et al 2006, Inhoff et al 2009) and gut motility (Fujimiya et al 2012), a GHS-R1a-independent antagonistic effect on ghrelin-induced insulin secretion and glucose metabolism, a trophic and protective effect on b-cells, as well as a role in muscle regeneration and in decreasing fat mass (Delhanty et al 2012, Delhanty & van der Lely 2013. How does unacylated ghrelin act?…”

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confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: Ghrelin/ghrelin receptors

Kaiya

Kangawa

Miyazato

2013

Journal of Molecular Endocrinology

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After the discovery in 1996 of the GH secretagogue-receptor type-1a (GHS-R1a) as an orphan G-protein coupled receptor, many research groups attempted to identify the endogenous ligand. Finally, Kojima and colleagues successfully isolated the peptide ligand from rat stomach extracts, determined its structure, and named it ghrelin. The GHS-R1a is now accepted to be the ghrelin receptor. The existence of the ghrelin system has been demonstrated in many animal classes through biochemical and molecular biological strategies as well as through genome projects. Our work, focused on identifying the ghrelin receptor and its ligand ghrelin in laboratory animals, particularly nonmammalian vertebrates, has provided new insights into the molecular evolution of the ghrelin receptor. In mammals, it is assumed that the ghrelin receptor evolution is in line with the plate tectonics theory. In contrast, the evolution of the ghrelin receptor in nonmammalian vertebrates differs from that of mammals: multiplicity of the ghrelin receptor isoforms is observed in nonmammalian vertebrates only. This multiplicity is due to genome duplication and polyploidization events that particularly occurred in Teleostei. Furthermore, it is likely that the evolution of the ghrelin receptor is distinct from that of its ligand, ghrelin, because only one ghrelin isoform has been detected in all species examined so far. In this review, we summarize current knowledge related to the molecular evolution of the ghrelin receptor in mammalian and nonmammalian vertebrates.

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mentioning

confidence: 99%

MOLECULAR EVOLUTION OF GPCRS: Ghrelin/ghrelin receptors

Kaiya

Kangawa

Miyazato

2013

Journal of Molecular Endocrinology

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“…У роботі P. Balagopal et al рівень греліну був достовірно нижчим у підлітків, хворих на ожиріння, порівняно із здоровими однолітками [24]. Дослід никами з Японії, що обстежували дітей з ожи-рінням, у третини з яких діагностували НАЖХП, виявлено нижчий рівень греліну в плазмі крові порівняно із здоровими [25]. Попередні дослідження показали, що у дітей з ожирінням порушується постпрандіальне зниження греліну [26].…”

Section: орексигенний гастроінтестинальний гормон грелін у патогенезіunclassified

Influence of Gastrointestinal Hormones on the Development of Obesity and Non-Alcoholic Fatty Liver Disease in Children

Parkhomenko¹,

Strashok²,

Khomenko³

2019

PEP

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Obesity is becoming a global epidemic among children, and the social significance of this problem is determined by the threat of disability of young patients, reducing life expectancy and the development of severe comorbidities. As a result of the increasing number of studies on energy homeostasis, it has been suggested that obesity is a multifactorial and more complex disease than previously thought. In recent years, the attention of researchers is increasingly attracted to the study of intestinal microbiota and its impact on human health, due to the development of new technologies and methods of studying the microbiome. Recent studies have shown that there is a mutual influence of the brain and intestines on each other, and there is increasing evidence that confirms the role of this complex relationship in the regulation of hunger, satiation and energy balance. It is proved that there is a direct impact on these processes of intestinal microbiota, and mediated through its intervention in the synthesis and metabolism of hormones and biologically active compounds of the digestive system. Today it is known that the gastrointestinal tract is one of the human organs where the most hormones are synthesized. At the present stage of development of science, it is known that there are more than 30 gastrointestinal hormones and biologically active substances that regulate the processes of digestion and participate in the regulation of general homeostasis. The most important role in the development of obesity and non-alcoholic fatty liver disease belongs to hormones such as ghrelin, peptide YY and glucagon-like peptide 1. The literature review presents current data that demonstrate the role of gastrointestinal hormones in the formation and development of obesity and non-alcoholic fatty liver disease in children as well as data of own research.

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Non-alcoholic fatty liver disease: a diabetologist’s perspective

et al. 2013

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In the recent years, non-alcoholic fatty liver disease (NAFLD) has emerged as the commonest cause of chronic liver disease in the developed world. The global epidemic of obesity secondary to physical inactivity and adverse food habits accounts for the alarming rise in NAFLD. Metabolic syndrome plays a major role in the pathogenesis of both NAFLD and type 2 diabetes mellitus (T2DM). Whilst most cases of NAFLD remain asymptomatic with only hepatic steatosis, about 30 % progress to non-alcoholic steatohepatitis with chronic liver inflammation that can lead on to fibrosis, cirrhosis, liver failure, and hepatocellular carcinoma. Because of the similar pathogenesis shared between T2DM and NAFLD, T2DM occurs as an important complication in many cases of NAFLD, and many cases of T2DM are further complicated by NAFLD. Rapid progression and increased complications of the individual diseases is the end result of this dual coexistence. Diagnosis of NAFLD relies upon hepatic imaging, serum biochemical markers, and liver biopsy. As in T2DM, the most important management option for patients with NAFLD is lifestyle changes targeted at weight reduction. Other treatment options include insulin sensitizers (metformin and pioglitazone), vitamin E, incretin mimetics, omega-3 fatty acids, cholesterol lowering agents, orlistat, and bariatric surgery. The clinical spectrum, patho-physiological features and therapeutic options of NAFLD share many things in common with T2DM and therefore, this review is to highlight the diabetologist's perspective of the disease.

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Ghrelin: a new treatment for non-alcoholic fatty liver disease?

Cited by 5 publications

References 11 publications

MOLECULAR EVOLUTION OF GPCRS: Ghrelin/ghrelin receptors

MOLECULAR EVOLUTION OF GPCRS: Ghrelin/ghrelin receptors

Influence of Gastrointestinal Hormones on the Development of Obesity and Non-Alcoholic Fatty Liver Disease in Children

Non-alcoholic fatty liver disease: a diabetologist’s perspective

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