scholarly journals Endocrine Disorders Accompanying Obesity - Effect or Cause?

2021 ◽  
Author(s):  
Alina Kurylowicz

Endocrine disorders including hypothyroidism and hypercortisolism are considered as causes of secondary obesity. However, several hormonal abnormalities can also be found in individuals with primary (simple) obesity. Part of them results from the adipose tissue dysfunction that, via secreted adipokines, modulates the function of endocrine organs and can be reversed with weight loss. However, part of them correspond to the real endocrine disorder and require appropriate treatment. Therefore in the management of obese patients, it is essential to distinguish between obesity-related abnormal results of hormonal tests and underlying endocrine disorder. This chapter presents pathophysiological concepts of obesity-related changes in the endocrine system and briefly reviews diagnostic algorithms helpful in distinguishing them from the co-existing endocrine disorders.


2012 ◽  
Vol 9 (4) ◽  
pp. 39-43 ◽  
Author(s):  
T I Romantsova ◽  
I V Poluboyarinova ◽  
O V Roik

Objective. To study the influence of the drug Reduxine in obese patients on the distribution of adipose tissue measured by MRI. Methods. In an open, prospective, non-randomized study duration of 20 weeks included 31 obese patients aged 20 to 65 years. During the study, the anthropometric parameters and the dynamics of the area of adipose tissue by means of MR imaging. Results. Weight loss in patients averaged 9.0 kg. Clinically significant weight loss reached 23 people (79%). Median reduction in waist circumference was 10 cm. Dynamic assessment of adipose tissue by MRI was performed in 17 patients. Reduxine treatment induced statistically significant decrease of both visceral and subcutaneous fat. Conclusions. According to the results of MRI, the reduction in waist circumference in patients receiving Reduxine occurred by reducing the number of both subcutaneous and visceral fat in the abdominal area.



2013 ◽  
Vol 169 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Anna De Rosa ◽  
Maria Ludovica Monaco ◽  
Mario Capasso ◽  
Pietro Forestieri ◽  
Vincenzo Pilone ◽  
...  

ObjectiveAdiponectin is an adipocytokine that exerts beneficial effects on obesity and related disorders by two receptors (ADIPORs). Adiponectin is produced as a monomer that circulates in serum as different oligomers. The oligomerization state and the tissue expression of adiponectin and ADIPORs are linked to its biological activities. In this study, the levels of total adiponectin and its oligomers were evaluated in relation to obesity and surgical weight loss. The expression of adiponectin and ADIPORs was analyzed in visceral and subcutaneous adipose tissues of obese patients.Design and methodsIn 25 obese patients and 44 age- and sex-matched controls, the serum levels of adiponectin and its oligomers were measured and compared by ELISA, western blotting, and gel filtration. The expression of adiponectin and ADIPORs in both adipose tissues was evaluated by real-time quantitative PCR and western blotting.ResultsThe amount of each adiponectin oligomer, including the monomer, increases after weight loss. The reduced circulating levels of adiponectin and its oligomers are not associated with the adipose tissue depot-specific expression of adiponectin and ADIPORs.ConclusionsOur results suggest that in patients, adiposity is associated with the serum concentrations of adiponectin and its oligomers but not with adipose tissue depot-specific expression of adiponectin and ADIPORs. In particular, the increase in adiponectin monomer levels could probably be related to the improvement of the whole-body energy metabolism then being involved in the improvement of adipose tissue function after weight loss. This work indicates the importance of assessing the whole adiponectin oligomeric profile as further potential indicators of adipose tissue functions in obesity.



2004 ◽  
Vol 183 (2) ◽  
pp. 331-342 ◽  
Author(s):  
Marcus Quinkler ◽  
Binayak Sinha ◽  
Jeremy W Tomlinson ◽  
Iwona J Bujalska ◽  
Paul M Stewart ◽  
...  

Women with polycystic ovary syndrome (PCOS) have high circulating androgens, thought to originate from ovaries and adrenals, and frequently suffer from the metabolic syndrome including obesity. However, serum androgens are positively associated with body mass index (BMI) not only in PCOS, but also in simple obesity, suggesting androgen synthesis within adipose tissue. Thus we investigated androgen generation in human adipose tissue, including expression of 17β-hydroxysteroid dehydrogenase (17β-HSD) isozymes, important regulators of sex steroid metabolism. Paired omental and subcutaneous fat biopsies were obtained from 27 healthy women undergoing elective abdominal surgery (age range 30–50 years; BMI 19.7–39.2 kg/m2). Enzymatic activity assays in preadipocyte proliferation cultures revealed effcient conversion of androstenedione to testosterone in both subcutaneous and omental fat. RT-PCR of whole fat and preadipocytes of subcutaneous and omental origin showed expression of 17β-HSD types 4 and 5, but no relevant expression of 17β-HSD types 1, 2, or 3. Microarray analysis confirmed this expression pattern (17β-HSD5>17β-HSD4) and suggested a higher expression of 17β-HSD5 in subcutaneous fat. Accordingly, quantitative real-time RT-PCR showed significantly higher expression of 17β-HSD5 in subcutaneous compared with omental fat (P<0.05). 17β-HSD5 expression in subcutaneous, but not omental, whole fat correlated significantly with BMI (r=0.51, P<0.05). In keeping with these findings, 17β-HSD5 expression in subcutaneous fat biopsies from six women taking part in a weight loss study decreased significantly with weight loss (P<0.05). A role for 17β-HSD5 in adipocyte differentiation was further supported by the observed increase in 17β-HSD5 expression upon differentiation of stromal preadipocytes to mature adipocytes (n=5; P<0.005), which again was higher in cells of subcutaneous origin. Functional activity of 17β-HSD5 also significantly increased with differentiation, revealing a net gain in androgen activation (androstenedione to testosterone) in subcutaneous cultures, contrasting with a net gain in androgen inactivation (testosterone to androstenedione) in omental cultures. Thus, human adipose tissue is capable of active androgen synthesis catalysed by 17β-HSD5, and increased expression in obesity may contribute to circulating androgen excess.



Author(s):  
Jorge-Luis Torres ◽  
Ricardo Usategui-Martín ◽  
Lourdes Hernández-Cosido ◽  
Edgar Bernardo ◽  
Laura Manzanedo-Bueno ◽  
...  

Abstract Background The peroxisome proliferator-activated receptor (PPAR)-γ plays a key role in adipose tissue differentiation and fat metabolism. However, it is unclear which factors may regulate its expression and whether obese patients have changes in adipose tissue expression of PPAR-γor potential regulators such as miR-27. Thus, our aims were to analyze PPAR-γ and miR-27 expression in adipose tissue of obese patients, and to correlate their levels with clinical variables. Subjects and Methods. We included 43 morbidly obese subjects who underwent sleeve gastrectomy (31 of them completed 1-year follow-up) and 19 non-obese subjects. mRNA expression of PPAR-γ1 and PPAR-γ2, miR-27a, and miR-27b was measured by qPCR in visceral and subcutaneous adipose tissue. Clinical variables and serum adipokine and hormone levels were correlated with PPAR-γ and miR-27 expression. In addition, a systematic review of the literature regarding PPAR-γ expression in adipose tissue of obese patients was performed. Results We found no differences in the expression of PPAR-γ and miR-27 in adipose tissue of obese patients vs. controls. The literature review revealed discrepant results regarding PPAR-γ expression in adipose tissue of obese patients. Of note, we described a significant negative correlation between pre-operative PPAR-γ1 expression in adipose tissue of obese patients and post-operative weight loss, potentially linked with insulin resistance markers. Conclusion PPAR-γ1 expression in adipose tissue is associated with weight loss after sleeve gastrectomy and may be used as a biomarker for response to surgery.



Author(s):  
Yvonne Corcoran

This chapter aims to explore the nursing skills required to care for the child and family with an underlying endocrine disorder both in a healthcare setting and in the community. This chapter will include an overview of the anatomy and physiology of the endocrine system, related pharmacology and microbiology, and a detailed description of the main skills involved in caring for children with an endocrine disorder and their families. Endocrine disorders in childhood are generally of a chronic nature, therefore prompt, accurate treatment and management are essential to ensure normal development into fully functioning adulthood. Disorders of the endocrine system can manifest their effects immediately or in a more gradual manner over days to months. Endocrine disorders most commonly occur due to three main reasons: a disordered endocrine system, often as a result of a genetic abnormality; overproduction of a particular hormone; or underproduction of a particular hormone (Evans & Tippins, 2008). Type 1 diabetes mellitus accounts for approximately 50% of endocrine disorders in childhood with an incidence in children (0–14 years) of 13.5 per 100,000 in the UK (Raine et al., 2006). Although some general principles apply to the nursing care of children with an endocrine disorder, you will need to refer to local policy and be familiar with local protocols regarding the nursing management of these children and their families in the hospital and the community. It is anticipated that you will be able to do the following once you have read and studied this chapter: ● Understand the anatomy and physiology of the endocrine system and how it affects many of our bodily functions. ● Understand the predominant pathological conditions related to the endocrine system. ● Understand the key nursing skills required to care for a child with an endocrine disorder and their family. The endocrine system is a chemical communi cation system that consists of hormone producing cells, hormones, and receptors (Glasper & Richardson, 2006). This system regulates and controls the body’s metabolic processes including energy production, growth, fluid and electrolyte balance, responses to stress, and sexual reproduction (Baxter et al., 2004).



2020 ◽  
Vol 9 (8) ◽  
pp. 2614
Author(s):  
Paula Juiz-Valiña ◽  
Lara Pena-Bello ◽  
Maria Cordido ◽  
Elena Outeiriño-Blanco ◽  
Sonia Pértega ◽  
...  

Endocrine disorders are common in obesity, including altered somatotropic axis. Obesity is characterized by reduced growth hormone (GH) secretion, although the insulin-like growth factor-1 (IGF-1) values are controversial. The aim of this study was to evaluate the effect of weight loss after bariatric surgery in the GH–IGF-1 axis in extreme obesity, in order to investigate IGF-1 values and the mechanism responsible for the alteration of the GH–IGF-1 axis in obesity. We performed an interventional trial in morbidly obese patients who underwent bariatric surgery. We included 116 patients (97 women) and 41 controls (30 women). The primary endpoint was circulating GH and IGF-1 values. Circulating IGF-1 values were lower in the obese patients than in the controls. Circulating GH and IGF-1 values increased significantly over time after surgery. Post-surgery changes in IGF-1 and GH values were significantly negatively correlated with changes in C-reactive protein (CRP) and free T4 values. After adjusting for preoperative body mass index (BMI), free T4 and CRP in a multivariate model, only CRP was independently associated with IGF-1 values in the follow-up. In summary, severe obesity is characterized by a functional hyposomatotropism at central and peripheral level that is progressively reversible with weight loss, and low-grade chronic inflammation could be the principal mediator.



Author(s):  
G. Catanzaro ◽  
T. Filardi ◽  
C. Sabato ◽  
A. Vacca ◽  
S. Migliaccio ◽  
...  

Abstract Background Obesity, characterized by an increased amount of adipose tissue, is a metabolic chronic alteration which has reached pandemic proportion. Lifestyle changes are the first line therapy for obesity and a large variety of dietary approaches have demonstrated efficacy in promoting weight loss and improving obesity-related metabolic alterations. Besides diet and physical activity, bariatric surgery might be an effective therapeutic strategy for morbid obese patients. Response to weight-loss interventions is characterised by high inter-individual variability, which might involve epigenetic factors. microRNAs have critical roles in metabolic processes and their dysregulated expression has been reported in obesity. Aim The aim of this review is to provide a comprehensive overview of current studies evaluating changes in microRNA expression in obese patients undergoing lifestyle interventions or bariatric surgery. Results A considerable number of studies have reported a differential expression of circulating microRNAs before and after various dietary and bariatric surgery approaches, identifying several candidate biomarkers of response to weight loss. Significant changes in microRNA expression have been observed at a tissue level as well, with entirely different patterns between visceral and subcutaneous adipose tissue. Interestingly, relevant differences in microRNA expression have emerged between responders and non-responders to dietary or surgical interventions. A wide variety of dysregulated microRNA target pathways have also been identified, helping to understand the pathophysiological mechanisms underlying obesity and obesity-related metabolic diseases. Conclusions Although further research is needed to draw firm conclusions, there is increasing evidence about microRNAs as potential biomarkers for weight loss and response to intervention strategies in obesity.



1970 ◽  
Vol 24 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Cathryn E. A. Hood ◽  
J. M. Goodhart ◽  
R. F. Fletcher ◽  
Josephine Gloster ◽  
P. V. Bertrand ◽  
...  

1. Diets containing 1000 kcal/day with varying proportions of carbohydrate (CHO) were fed to four women with simple obesity. The patients were given, in various sequences and for 8 days in each instance, diets in which 3, 6, 12, 25 or 50% of the calories were supplied by sucrose.2. No significant difference in the rate of weight loss was found when the diets of graded CHO content were fed and mean weight loss was 1.2 kg/week.3. The high-CHO diets were antiketogenic; there was no daily relationship between urinary ketones and sodium. The 25 and 50% CHO diets had a nitrogen-sparing effect.4. A 1000 kcal/day diet with about a third of the calories derived from CHO leads to a useful rate of weight loss and minimum changes in body chemistry. This finding may have implications in the long-term treatment of obesity.



2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Timon E. Adolph ◽  
Felix Grabherr ◽  
Lisa Mayr ◽  
Christoph Grander ◽  
Barbara Enrich ◽  
...  

Introduction. Obesity and related nonalcoholic fatty liver disease (NAFLD) are an emerging health care issue that imposes substantial morbidity to individuals. Growth and differentiation factor 15 (GDF15) limits food uptake, body weight, and energy balance by modulation of GDNF-family receptor α-like (GFRAL) signalling in the hindbrain. However, the regulation of GDF15 expression in obesity and NAFLD is incompletely understood. We sought to define the impact of weight loss achieved by laparoscopic adjustable gastric banding (LAGB) on hepatic and adipose GDF15 expression in a cohort of severely obese patients. Methods. We analysed GDF15 expression of liver and subcutaneous adipose tissue before and 6 months after LAGB in severely obese patients undergoing LAGB by quantitative real-time PCR. To assess the role of inflammation on GDF15 expression, we analysed Hep G2 hepatocytes stimulated with cytokines such as IL-1β, TNFα, IL-6, LPS, or cellular stressors such as tunicamycin. Results. GDF15 expression was mostly confined to the liver compared to adipose tissue in severely obese patients. Weight loss induced by LAGB was associated with reduced hepatic (but not adipose tissue) expression of GDF15. Stimulation with IL-1β or tunicamycin induced hepatic GDF15 expression in hepatocytes. In line with this, hepatic GDF15 expression directly correlated with IL-1β expression and steatosis severity in NAFLD. These data demonstrated that amelioration of metabolic inflammation and weight loss reduced hepatic GDF15 expression. Conclusion. Based on recent mechanistic findings, our data suggest that hepatic GDF15 may serve as a negative feedback mechanism to control energy balance in NAFLD.



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