Decrease in leptin production by the adipose tissue in obesity associated with severe metabolic syndrome

Paz-Filho, Gilberto; Volaco, Alexei; Suplicy, Henrique Lacerda; Radominski, Rosana Bento; Boguszewski, César Luiz

doi:10.1590/s0004-27302009000900005

Cited by 37 publications

(24 citation statements)

References 54 publications

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“…The blood samples for laboratory tests were collected after a 12-hour fast and immediately placed on ice, centrifuged at 4°C, and stored at -80°C. Measurement of serum leptin, adiponectin, and monocyte chemoattractant protein-1 (MCP-1) were performed by enzyme immunoassay (ELISA, Quantikine RDSY-DLP00 and RDSY-DRP300, R & D Systems, Minneapolis, MN, USA) and the results were adjusted according to the participants' fat mass, assessed by dual-energy X-ray absorption (DXA; Lunar Prodigy Advance, GE Healthcare, Pittsburgh, PA, USA) (12). Additionally, we measured CRP levels by nephelometry (Siemens BNII, Munich, Germany; minimum detection level 0.1 mg/dL).…”

Section: Methodsmentioning

confidence: 99%

Serum levels of leptin and adiponectin and clinical parameters in women with fibromyalgia and overweight/obesity

Paiva

Andretta

Batista

et al. 2017

Arch. Endocrinol. Metab.

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Objectives: The objectives of this study were to evaluate the serum levels of adipokines in women with fibromyalgia with and without overweight/obesity, and to correlate the adipokines levels with clinical parameters associated with fibromyalgia and adipose tissue mass (body fat). Subjects and methods: The study included 100 women divided into four groups: (a) fibromyalgia and overweight/obesity; (b) fibromyalgia and normal weight; (c) controls and overweight/obesity; and (d) controls and normal weight. Patients and controls were evaluated for clinical, anthropometric, and fibromyalgia-related parameters. Assessments included serum levels of leptin, adiponectin, monocyte chemoattractant protein-1 (MCP-1), and C-reactive protein (CRP). Levels of adipokines were further adjusted for fat mass. Results: Fibromyalgia patients with overweight/obesity or normal weight had no differences in clinical parameters. Unadjusted leptin levels were lower in fibromyalgia patients than controls, a finding that was more remarkable in fibromyalgia patients with overweight/obesity. Leptin levels had no correlation with clinical parameters of fibromyalgia or inflammation markers (MCP-1 and CRP), and adiponectin levels showed no difference between groups. Conclusions: No correlation was observed between adjusted leptin levels and clinical parameters of fibromyalgia. Patients with fibromyalgia and overweight/obesity presented lower levels of leptin than controls with overweight/ obesity. Arch Endocrinol Metab. 2017;61(3):249-56.

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Section: Methodsmentioning

confidence: 99%

Serum levels of leptin and adiponectin and clinical parameters in women with fibromyalgia and overweight/obesity

Paiva

Andretta

Batista

et al. 2017

Arch. Endocrinol. Metab.

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“…Th is resistance may be secondary to obesity or vice versa, and genetic factors, age, diet, sedentary lifestyle, and stress might contribute to the development of defects in the transport of leptin across the BBB or might lead to abnormalities in leptin signaling (Paz-Filho et al 2009). …”

Section: Role Of Peripheral Adiposity Signalsmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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“…Leptin is associated with insulin resistance and metabolic syndrome independent of obesity via central obesity, possibly by impairment of insulin signaling at the insulin receptor substrate 1 phosphorylation (51). Leptin is increased in patients with metabolic syndrome, but relative hypoleptinemia may be observed in cases of severe metabolic syndrome, possibly due to adipose tissue dysfunction (52).…”

Section: Hyperleptinemic States: Obesity and Metabolic Syndromementioning

confidence: 99%

Leptin: molecular mechanisms, systemic pro-inflammatory effects, and clinical implications

Paz-Filho

Mastronardi

Franco

et al. 2012

Arq Bras Endocrinol Metab

179

148

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SUMMARYLeptin, the adipokine produced mainly by the white adipose tissue, plays important roles not only in the regulation of food intake, but also in controlling immunity and inflammation. It has been widely demonstrated that the absence of leptin leads to immune defects in animal and human models, ultimately increasing mortality. Leptin also regulates inflammation by means of actions on its receptor, that is widely spread across different immune cell populations. The molecular mechanisms by which leptin determines its biological actions have also been recently elucidated, and three intracellular pathways have been implicated in leptin actions: JAK-STAT, PI3K, and ERK 1/2. These pathways are closely regulated by intracellular proteins that decrease leptin biological activity. In this review, we discuss the molecular mechanisms by which leptin regulates immunity and inflammation, and associate those mechanisms with chronic inflammatory disorders. Arq Bras Endocrinol Metab. 2012;56(9):597-607 Keywords Leptin; immunity; inflammation; cytokines SUMÁRIO A leptina, uma adipocina produzida principalmente pelo tecido adiposo branco, tem um papel importante não somente na regulação da ingestão alimentar, mas também no controle da imunidade e da inflamação. Já foi amplamente demonstrado que a ausência de leptina causa deficiências imunológicas em modelos animais e em humanos, levando ao aumento da mortalidade. A leptina também regula a inflamação por meio da ação em seu receptor, amplamente distribuído em diversos tipos de células do sistema imunológico. Os mecanismos moleculares pelos quais a leptina determina suas ações biológicas foram recentemente elucidados, e três cascatas intracelulares são ativadas pela leptina: JAK-STAT, PI3K e ERK 1/2. Essas cascatas são reguladas por proteínas intracelulares, reduzindo as ações da leptina. Nesta revisão, são discutidos os mecanismos moleculares pelos quais a leptina regula a imunidade e a inflamação, associando-os a enfermidades inflamatórias crônicas. Arq Bras Endocrinol Metab. 2012;56(9):597-607 Descritores

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Decrease in leptin production by the adipose tissue in obesity associated with severe metabolic syndrome

Abstract: Leptin production by the adipose tissue is decreased in obese subjects fulfilling three or more criteria of MetS, suggesting a state of relative leptin deficiency in obesity associated with advanced stages of MetS.

Cited by 37 publications

References 54 publications

Serum levels of leptin and adiponectin and clinical parameters in women with fibromyalgia and overweight/obesity

Serum levels of leptin and adiponectin and clinical parameters in women with fibromyalgia and overweight/obesity

Central and peripheral control of food intake

Leptin: molecular mechanisms, systemic pro-inflammatory effects, and clinical implications

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