Novel Molecular Aspects of Ghrelin and Leptin in the Control of Adipobiology and the Cardiovascular System

Rodríguez, Amaia

doi:10.1159/000360837

Cited by 45 publications

(22 citation statements)

References 110 publications

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“…It has also been proven that fasting plasma ghrelin values in obese patients inversely correlate with plasma leptin concentrations [28,29]. However, recent research has proposed that the two systems might work independently of each other, with different pathophysiological mechanisms [30]. Our finding of a correlation between adiponectin and ghrelin in all three research groups will require confirmation in other studies and further research.…”

Section: Discussionsupporting

confidence: 52%

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

2020

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Introduction: The occurrence of cardiovascular diseases and metabolic disorders steadily increases with the body mass index (BMI). Since the latter is not the best and earliest indicator of obesity and cardiovascular risk, the aim of the study was to evaluate some potential biological markers that would allow us to detect children and adolescents at higher risk at an early stage. Methods: A sample of 330 children and adolescents were included in the study and divided into four groups: obese patients with hypertension, normal-weight patients with hypertension, patients with mildly elevated lipids and a control group of healthy children and adolescents. Some clinical parameters (age, body weight, body height, BMI, waist circumference, hip circumference, blood pressure), biochemical parameters (glucose, total cholesterol, triglycerides, HDL, LDL, apolipoprotein A1, homocysteine) and biological markers of obesity (ghrelin, adiponectin, leptin) were evaluated. Results: Ghrelin and adiponectin were found to have a strong negative statistically significant correlation with BMI in all three observed groups (p < 0.001), but not in the control group (p = 0.053 and p = 0.316, respectively). In addition, leptin had a strong positive statistically significant correlation with BMI in all four groups (p < 0.001 for the research groups, p = 0.009 for the controls). In the group of obese patients with hypertension, statistically significant differences in all three markers of obesity were found in comparison to the control group (p < 0.001 for all markers). In the group of patients with mildly elevated lipids, ghrelin and leptin were significantly different (p = 0.002 and p < 0.001, respectively). In the group of normal-weight hypertensive patients, only values of ghrelin were different compared to the control group (p = 0.001). Conclusion: In the research groups, significant differences were found in clinical, biochemical and biological parameters compared to the control group. The observed biological markers of obesity are useful early markers for identifying groups of patients that are at cardiovascular risk.

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Section: Discussionsupporting

confidence: 52%

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

2020

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“…Leptin is an adipokine that reduces food intake and increases energy expenditure to maintain energy balance 33 . As expected, leptin-deficient ob/ob mice exhibited severe obesity and hyperphagia ( Table 1 ).…”

Section: Resultsmentioning

confidence: 99%

Leptin administration restores the altered adipose and hepatic expression of aquaglyceroporins improving the non-alcoholic fatty liver of ob/ob mice

Rodríguez

Moreno

Balaguer

et al. 2015

Sci Rep

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Glycerol is an important metabolite for the control of lipid accumulation in white adipose tissue (WAT) and liver. We aimed to investigate whether exogenous administration of leptin improves features of non-alcoholic fatty liver disease (NAFLD) in leptin-deficient ob/ob mice via the regulation of AQP3 and AQP7 (glycerol channels mediating glycerol efflux in adipocytes) and AQP9 (aquaglyceroporin facilitating glycerol influx in hepatocytes). Twelve-week-old male wild type and ob/ob mice were divided in three groups as follows: control, leptin-treated (1 mg/kg/d) and pair-fed. Leptin deficiency was associated with obesity and NAFLD exhibiting an AQP3 and AQP7 increase in WAT, without changes in hepatic AQP9. Adipose Aqp3 and hepatic Aqp9 transcripts positively correlated with markers of adiposity and hepatic steatosis. Chronic leptin administration (4-weeks) was associated with improved body weight, whole-body adiposity, and hepatosteatosis of ob/ob mice and to a down-regulation of AQP3, AQP7 in WAT and an up-regulation of hepatic AQP9. Acute leptin stimulation in vitro (4-h) induced the mobilization of aquaglyceroporins towards lipid droplets (AQP3) and the plasma membrane (AQP7) in murine adipocytes. Our results show that leptin restores the coordinated regulation of fat-specific AQP7 and liver-specific AQP9, a step which might prevent lipid overaccumulation in WAT and liver in obesity.

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“…Ghrelin can regulate GH release, food intake, adiposity, and energy metabolism. It promotes adiposity by the activation of hypothalamic orexigenic neurons and stimulates the expression of several fat storage-related proteins in adipocytes, thereby stimulating lipid accumulation [ 93 ]. In obese children, AG levels and AG:obestatin ratio are significantly lower, and AG is negatively correlated with triglyceride (TG), low-density lipoprotein-C, insulin, and homeostatic model assessment of insulin resistance [ 94 ].…”

Section: Ghrelin and Lipid Metabolismmentioning

confidence: 99%

Ghrelin, a gastrointestinal hormone, regulates energy balance and lipid metabolism

Liang

Wang

et al. 2018

Bioscience Reports

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Ghrelin, an acylated peptide hormone of 28 amino acids, is an endogenous ligand of the released growth hormone secretagogue receptor (GHSR). Ghrelin has been isolated from human and rat stomach and is also detected in the hypothalamic arcuate nucleus. Ghrelin receptor is primarily located in the neuropeptide Y and agouti-related protein neurons. Many previous studies have shown that ghrelin and GHSR are involved in the regulation of energy homeostasis, and its administration can increase food intake and body weight gain. AMP-activated protein kinase is activated by ghrelin in the hypothalamus, which contributes to lower intracellular long-chain fatty acid level. Ghrelin appears to modulate the response to food cues via a neural network involved in the regulation of feeding and in the appetitive response to food cues. It also increases the response of brain areas involved in visual processing, attention, and memory to food pictures. Ghrelin is also an important factor linking the central nervous system with peripheral tissues that regulate lipid metabolism. It promotes adiposity by the activation of hypothalamic orexigenic neurons and stimulates the expression of fat storage-related proteins in adipocytes. Meanwhile, ghrelin exerts direct peripheral effects on lipid metabolism, including increase in white adipose tissue mass, stimulation of lipogenesis in the liver, and taste sensitivity modulation.

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Novel Molecular Aspects of Ghrelin and Leptin in the Control of Adipobiology and the Cardiovascular System

Cited by 45 publications

References 110 publications

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

The associations between some biological markers, obesity, and cardiovascular risk in Slovenian children and adolescents

Leptin administration restores the altered adipose and hepatic expression of aquaglyceroporins improving the non-alcoholic fatty liver of ob/ob mice

Ghrelin, a gastrointestinal hormone, regulates energy balance and lipid metabolism

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