Role of the Ghrelin and the Leptin Levels in the Regulation of Body Weight in the Patients with Metabolic Syndrome

10.12737/3309 ◽  
2014 ◽  
Vol 21 (1) ◽  
pp. 36-38
Author(s):  
Корнеева ◽  
E. Korneeva

The variety of metabolic functions of protein hormones - leptin and ghrelin - determines the difference in the therapeutic approach to the treatment of patients with metabolic syndrome. This paper presents the results of a study of the leptin and ghrelin levels in serum of patients with metabolic syndrome. It was revealed that hyperleptinemia was observed in 20.2% of patients with the most obese women II and III than in men. Leptin resistance is also more common in women than in men by 36.4%. However, the ratio of leptin / BMI against compliance with the recommendations for the treatment of metabolic syndrome in men decreased by 2.1 times faster than that of women. Ghrelin levels remained high in patients with the metabolic syndrome by obesity III and IV degree after ingestion. In these patients the strength of lowering the ghrelin level is proportional to time. The rate of gastric emptying was delayed , and the feeling of satiety did not come. This has contributed to an increase in the amount of food intake and body weight gain at the expense of adipose tissue , producing high levels of leptin. The continued high drop it ghrelin and leptin in serum of obese patients significantly impede range of therapeutic interventions.

2006 ◽  
Vol 291 (5) ◽  
pp. E1038-E1043 ◽  
Author(s):  
Petra Kok ◽  
Ferdinand Roelfsema ◽  
Marijke Frölich ◽  
Johannes van Pelt ◽  
Marcel P. M. Stokkel ◽  
...  

The metabolic syndrome comprises a cluster of metabolic anomalies including insulin resistance, abdominal obesity, dyslipidemia, and hypertension. Previous studies suggest that impaired dopamine D2 receptor (D2R) signaling is involved in its pathogenesis. We studied the acute effects of bromocriptine (a D2R agonist) on energy metabolism in obese women; body weight and caloric intake remained constant. Eighteen healthy, obese women (BMI 33.2 ± 0.6 kg/m2, mean age 37.5 ± 1.7, range 22–51 yr) were studied twice in the follicular phase of their menstrual cycle in a prospective, single-blind, crossover design. Subjects received both placebo (P; always first occasion) and bromocriptine (B; always second occasion) on separate occasions for 8 days. At each occasion blood glucose and insulin were assessed every 10 min for 24 h, and circadian plasma free fatty acid (FFA) and triglyceride (TG) levels were measured hourly. Fuel oxidation was determined by indirect calorimetry. Body weight and composition were not affected by the drug. Mean 24-h blood glucose ( P < 0.01) and insulin ( P < 0.01) were significantly reduced by bromocriptine, whereas mean 24 h FFA levels were increased ( P < 0.01), suggesting that lipolysis was stimulated. Bromocriptine increased oxygen consumption ( P = 0.03) and resting energy expenditure (by 50 kcal/day, P = 0.03). Systolic blood pressure was significantly reduced by bromocriptine. Thus these results imply that short-term bromocriptine treatment ameliorates various components of the metabolic syndrome while it shifts energy balance away from lipogenesis in obese humans.


2013 ◽  
Vol 10 (1) ◽  
pp. 27-38 ◽  
Author(s):  
Christina Chrysohoou ◽  
Demosthenes Panagiotakos ◽  
Christos Pitsavos ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Anikó Pósa ◽  
Renáta Szabó ◽  
Krisztina Kupai ◽  
Anett Csonka ◽  
Zita Szalai ◽  
...  

The estrogen deficiency after menopause leads to overweight or obesity, and physical exercise is one of the important modulators of this body weight gain. Female Wistar rats underwent ovariectomy surgery (OVX) or sham operation (SO). OVX and SO groups were randomized into new groups based on the voluntary physical activity (with or without running) and the type of diet for 12 weeks. Rats were fed standard chow (CTRL), high triglyceride diet (HT), or restricted diet (CR). The metabolic syndrome was assessed by measuring the body weight gain, the glucose sensitivity, and the levels of insulin, triglyceride, leptin, and aspartate aminotransferase transaminase (AST) and alanine aminotransferase (ALT). The exercise training combined with the CR resulted in improvements in the glucose tolerance and the insulin sensitivity. Plasma TG, AST, and ALT levels were significantly higher in OVX rats fed with HT but these high values were suppressed by exercise and CR. Compared to SO animals, estrogen deprivation with HT caused a significant increase in leptin level. Our data provide evidence that CR combined with voluntary physical exercise can be a very effective strategy to prevent the development of a metabolic syndrome induced by high calorie diet.


INTRODUCTION Alzheimer’s disease (AD) is characterized by progressive cognitive loss coupled with age-related functional impairment. Its two major brands are β-amyloid plaques and neurofibrillary tangles. There is strong evidence for a relationship between Metabolic Syndrome (MS) and AD. Both pathologies are quite prevalent and dependent on aging. OBJECTIVE The present study seeks to understand the role of the metabolic syndrome in the pathophysiology of Alzheimer’s disease and to describe preventive and therapeutic interventions. METHODOLOGY The review was made based on the search for scientific articles in the electronic databases PUBMED and Web of Science, using the descriptors “Alzheimer’s Disease”, “Metabolic Syndrome” DISCUSSION MS is a metabolic breakdown with the potential to damage insulin signaling in the brain, causing insulin resistance, inhibiting β-amyloid clearance and its accumulation, which generates neuroinflammation. In addition, it induces a prothrombotic state with ischemic effects, resulting in oxidative stress and neuroinflammation and progressive local brain atrophies. The components of the metabolic syndrome are related to AD, exacerbating neuroinflammation and insulin resistance. Preventive and therapeutic measures aiming at the MS are promising. CONCLUSION From the analyzes developed in this study, different relationships between the components of MS and AD are perceived, the first being possible causes and / or effects of the second. Since insulin resistance plays a major role in the initiation and perpetuation of cognitive impairment in AD. Furthermore, the components of MS associated with AD, when treated with preventive and therapeutic measures, break this association by promoting rebalancing of the metabolism.


2018 ◽  
Vol 315 (4) ◽  
pp. G602-G617 ◽  
Author(s):  
Erika Tarasco ◽  
Giovanni Pellegrini ◽  
Lynda Whiting ◽  
Thomas A. Lutz

The metabolic syndrome (MetS) is a major health issue worldwide and is associated with obesity, insulin resistance, and hypercholesterolemia. Several animal models were used to describe the MetS; however, many of them do not mimic well the MetS pathophysiology in humans. The ApoE*3Leiden.CETP mouse model overcomes part of this limitation, since they have a humanised lipoprotein metabolism and a heterogeneous response to MetS, similar to humans. The reported heterogeneity among them and their common classification refer to responder (R) and nonresponder (NR) mice; R mice show increased body weight, cholesterol, and triglycerides levels, whereas NR mice do not show this expected phenotype when fed a Western type diet. To define better the differences between R and NR mice, we focused on feeding behavior, body weight gain, glucose tolerance, and lipid parameters, and on an extensive pathological examination along with liver histology analysis. Our data confirmed that R mice resemble the pathological features of the human MetS: obesity, dysplipidemia, and glucose intolerance. NR mice do not develop the full dysmetabolic phenotype because of a severe inflammatory hepatic condition, which may heavily affect liver function. We conclude that R and NR mice are metabolically different and that NR mice have indications of severely impaired liver function. Hence, it is critical to identify and separate the respective mice to decrease data heterogeneity. Clinical chemistry and histological analysis should be used to confirm retrospectively the animals’ classification. Moreover, we point out that NR mice may not be an appropriate control for studies involving ApoE*3Leiden.CETP R mice. NEW & NOTEWORTHY When compared with some other animal models, ApoE*3Leiden.CETP mice are better models to describe the metabolic syndrome. However, there is phenotypic heterogeneity between “responder” and “nonresponder” mice, the latter showing some evidence of hepatic pathology. A full phenotypic characterization and eventually postmortem analysis of the liver are warranted.


2010 ◽  
Vol 103 (04) ◽  
pp. 788-796 ◽  
Author(s):  
Isabel Platzer ◽  
Sandra Ernst ◽  
Carina Walter ◽  
Philipp Rudolf ◽  
Katja Zirlik ◽  
...  

SummaryCD40L figures prominently in atherogenesis. Recent data demonstrate elevated levels of sCD40L in the serum of patients with the metabolic syndrome (MS). This study investigated the role of CD40L in pro-inflammatory gene expression and cellular differentiation in adipose tissue to obtain insight into mechanisms linking the MS with atherosclerosis. Human adipocytes and preadipocytes expressed CD40 but not CD40L. Stimulation with recombinant CD40L or membranes over-expressing CD40L induced a time- and dose-dependent expression of IL-6, MCP-1, IL-8, and PAI-1. Supernatants of CD40L-stimulated adipose cells activated endothelial cells, suggesting a systemic functional relevance of our findings. Neutralising antibodies against CD40L attenuated these effects substantially. Signalling studies revealed the involvement of mitogen-activated protein kinases and NFκB. Furthermore, stimulation with CD40L resulted in enhanced activation of C/EBPα and PPARγ and promoted adipogenesis of preadipose cells in the presence and absence of standard adipogenic conditions. Finally, patients suffering from the metabolic syndrome with high levels of sCD40L also displayed high levels of IL-6, in line with the concept that CD40L may induce the expression of inflammatory cytokines in vivo in this population. Our data reveal potent metabolic functions of CD40L aside from its known pivotal pro-inflammatory role within plaques. Our data suggest that CD40L may mediate risk at the interface of metabolic and atherothrombotic disease.


Author(s):  
Elena Korneeva ◽  
Mikhail Voevoda ◽  
Sergey Semaev ◽  
Vladimir Maksimov

Results of the study related to polymorphism of ACE gene (rs1799752)‎, integrin αIIbβ3, and CSK gene (rs1378942) influencing development of arterial hypertension in young patients with metabolic syndrome are presented. Hypertension as a component of the metabolic syndrome was detected in 15.0% of young patients. Prevalence of mutant alleles of the studied genes among the examined patients was quite high, so homozygous DD genotype was found in 21.6%, and mutant D allele of the ACE gene in 47.4%. A high risk of hypertension in patients with MS was detected in carriers of the T allele of the CSK (rs1378942) gene – 54.8%, which was most often observed in a combination of polymorphic ACE and CSK gene loci (p = 0.0053).


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