scholarly journals Obesity — a genetic disease of adipose tissue?

2000 ◽  
Vol 83 (S1) ◽  
pp. S9-S16 ◽  
Author(s):  
Peter Arner
Keyword(s):  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Uncoupling Protein 1 ◽  
Necrosis Factor Alpha ◽  
Density Lipoprotein Receptor ◽  
Factor Alpha ◽  
Obesity Genes ◽  
Necrosis Factor

Although the rapid increase in the prevalence of obesity in many countries suggests that environmental factors (mainly overeating and physical inactivity) play the most important role in the development of overweight, it is very likely that genetic factors also contribute. It appears that one major gene in combination with one or several minor genes constitute the genetic components behind excess accumulation of body fat in most obese individuals. However, monogenic obesity has been described in a few families due to changes in leptin, leptin receptor, prohormone convertase, pro-opiomelanocortin or melanocortin-4 receptor. None of the monogenic variants is of great importance for common human obesity; the latter genes are unknown so far. Results from genomic scans suggest that major obesity genes are located on chromosomes 2, 10, 11 and 20. Studies of candidate genes indicate that the minor obesity genes control important functions of adipose tissue, and that structural variance in these genes may alter adipose tissue function in a way that promotes obesity. Such genes are β2- and β3-adrenoceptors, hormone-sensitive lipase, tumour necrosis factor alpha, uncoupling protein-1, low-density lipoprotein receptor, and peroxisome proliferator activator receptor gamma-2. Some of these genes may promote obesity by gene–gene interactions (for example β3-adrenoceptors and uncoupling protein-1) or gene–environment interactions (for example β2-adrenoceptors and physical activity). Some are important for obesity only among women (for example β2- and β3-adrenoceptors, low-density lipoprotein receptor and tumour necrosis factor alpha). Few ‘non-adipose’ genes have so far shown a firm association to common human obesity, which could suggest that the important genes for the development of excess body fat also control adipose tissue function.

The relationship between adenovirus-36 seropositivity, obesity and metabolic profile in Turkish children and adults

2015 ◽  
Vol 143 (16) ◽  
pp. 3550-3556 ◽  
Author(s):  
M. KARAMESE ◽  
U. ALTOPARLAK ◽  
A. TURGUT ◽  
S. AYDOGDU ◽  
S. AKSAK KARAMESE
Keyword(s):  
Tumour Necrosis ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Tumour Necrosis Factor Alpha ◽  
Obese Children ◽  
Necrosis Factor Alpha ◽  
Adults And Children ◽  
Factor Alpha ◽  
Adenovirus 36 ◽  
Necrosis Factor

SUMMARYObesity potentially arising from viral infection is known as ‘infectobesity’. The latest reports suggest that adenovirus-36 (Adv36) is related to obesity in adults and children. Our aim was not only to determine the Adv36 seropositivity in both obese and non-obese children and adults, but also to investigate correlations between antibody positivity and serum lipid profiles. Both Adv36 positivity and tumour-necrosis-factor-alpha, leptin and interleukin-6 levels were detected in blood samples collected from 146 children and 130 adults by ELISA. Fasting plasma triglycerides, total cholesterol and low-density lipoprotein levels were also measured. Adv36 positivity was determined to be 27·1% and 6% in obese and non-obese children and 17·5% and 4% in obese and non-obese adults, respectively. There was no difference with regard to total cholesterol, low-density lipoprotein, triglyceride, tumour-necrosis-factor-alpha and interleukin-6 levels (P> 0·05). However, there was a significant difference between groups in terms of leptin levels (P< 0·05). We determined the prevalence of Adv36 positivity in obese children and adults. Our results showed that Adv36 may be an obesity agent for both adults and children, parallel with current literature data. However, the available data on a possible relationship between Adv36 infection and obesity both in children and adults do not completely solve the problem.

scholarly journals Correlation of Small Dense Low Density Lipoprotein, Tumour Necrosis Factor - alpha with Liver Enzymes in Chronic Hepatitis B Patients

2019 ◽  
pp. 1-8
Author(s):  
Isaac Oluwole Adediji ◽  
Adeolu Sunday Oluremi ◽  
Ayodele Ademola Adelakun ◽  
Paul Olusegun Adepoju ◽  
Dominion Akingbade ◽  
...  
Keyword(s):  
Chronic Hepatitis ◽  
Hepatitis B ◽  
Chronic Hepatitis B ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
The Relationship ◽  
Necrosis Factor

Aim: This study investigated the relationship between small dense low density lipoprotein (sdLDL), tumour necrosis factor-alpha (TNF-α), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) in chronic hepatitis B patients. Duration of Study: June 2018- March 2019. Subjects and Methods: Sixty (60) participants were recruited for this cross sectional study. They comprised thirty (30) clinically diagnosed chronic hepatitis B virus (HBV) infected patients attending clinic at a tertiary hospital in Osogbo, Osun state, Nigeria. Thirty (30) apparently healthy volunteers were recruited as control subjects after fulfilling the inclusion criteria. Anthropometric measurements were performed using standard method. About 6mL of venous blood was collected from each study participant, serum was extracted and kept at -80oC until time of analysis. Small dense LDL, TNF-α, AST, ALT and ALP were determined using enzyme linked immunosorbent assay and colorimetric method as appropriate. Data analysis was done using Student’s t-test for comparison of variables and Pearson’s correlation was used to determine the relationship between variables. P–value less than 0.05 was considered significant.   Results: SdLDL, TNF-α, AST and ALT were significantly elevated in HBV patients when compared with the control subjects (P<0.05). SdLDL had a significant positive correlation with TNF-α (P=0.03), AST (P=0.01), ALT (P=0.00). TNF-α had a significant positive correlation with AST (P=0.02) and ALT (P=0.00). Conclusion: This study revealed a noteworthy positive relationship between sdLDL, TNF-α and hepatic aminotransferases in chronic hepatitis B patients.

scholarly journals Low-density lipoprotein receptor-related protein 1 (LRP1) is a novel receptor for apolipoprotein A4 (APOA4) in adipose tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jie Qu ◽  
Sarah Fourman ◽  
Maureen Fitzgerald ◽  
Min Liu ◽  
Supna Nair ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Molecular Mechanisms ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Receptor ◽  
Dependent Manner ◽  
Related Protein ◽  
Density Lipoprotein Receptor ◽  
Lipoprotein Receptor Related Protein

AbstractApolipoprotein A4 (APOA4) is one of the most abundant and versatile apolipoproteins facilitating lipid transport and metabolism. APOA4 is synthesized in the small intestine, packaged onto chylomicrons, secreted into intestinal lymph and transported via circulation to several tissues, including adipose. Since its discovery nearly 4 decades ago, to date, only platelet integrin αIIbβ3 has been identified as APOA4 receptor in the plasma. Using co-immunoprecipitation coupled with mass spectrometry, we probed the APOA4 interactome in mouse gonadal fat tissue, where ApoA4 gene is not transcribed but APOA4 protein is abundant. We demonstrate that lipoprotein receptor-related protein 1 (LRP1) is the cognate receptor for APOA4 in adipose tissue. LRP1 colocalized with APOA4 in adipocytes; it interacted with APOA4 under fasting condition and their interaction was enhanced during lipid feeding concomitant with increased APOA4 levels in plasma. In 3T3-L1 mature adipocytes, APOA4 promoted glucose uptake both in absence and presence of insulin in a dose-dependent manner. Knockdown of LRP1 abrogated APOA4-induced glucose uptake as well as activation of phosphatidylinositol 3 kinase (PI3K)-mediated protein kinase B (AKT). Taken together, we identified LRP1 as a novel receptor for APOA4 in promoting glucose uptake. Considering both APOA4 and LRP1 are multifunctional players in lipid and glucose metabolism, our finding opens up a door to better understand the molecular mechanisms along APOA4-LRP1 axis, whose dysregulation leads to obesity, cardiovascular disease, and diabetes.

scholarly journals Increased adipose tissue secretion of interleukin-6, but not of leptin, plasminogen activator inhibitor-1 or tumour necrosis factor alpha, in Graves' hyperthyroidism

2002 ◽  
pp. 607-611 ◽  
Author(s):  
H Wahrenberg ◽  
A Wennlund ◽  
J Hoffstedt
Keyword(s):  
Adipose Tissue ◽  
Plasminogen Activator Inhibitor ◽  
Tumour Necrosis Factor Alpha ◽  
Tnf Alpha ◽  
Plasminogen Activator Inhibitor 1 ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Activator Inhibitor ◽  
Necrosis Factor ◽  
Pai 1

OBJECTIVE: This study was designed to investigate adipose tissue secretion of interleukin-6 (IL-6), leptin, tumour necrosis factor alpha (TNF-alpha) and plasminogen activator inhibitor-1 (PAI-1) in Graves' hyperthyroidism. DESIGN: We studied 10 patients before and during (after 8 weeks) anti-thyroid treatment for Graves' hyperthyroidism and 16 healthy, euthyroid control subjects. METHODS: Plasma levels of thyroid hormones and serum/plasma levels of IL-6, leptin, TNF-alpha and PAI-1 were analysed. Subcutaneous fat biopsies were taken for subsequent measurement of IL-6, leptin, TNF-alpha and PAI-1 protein secretion. RESULTS: In patients with Graves' disease, the anti-thyroid treatment resulted in significant reductions of plasma thyroxine and triiodothyronine levels. No differences in serum concentration or adipose tissue secretion of leptin or TNF-alpha were observed either before, as compared with during, anti-thyroid treatment, or in comparison with euthyroid controls. In contrast, plasma PAI-1 activity, but not adipose tissue secretion of PAI-1, was increased both in Graves' disease before as compared with during anti-thyroid treatment (P=0.01) and in thyrotoxic patients compared with euthyroid controls (P=0.0001). Finally, adipose secretion of IL-6 was increased both before (8-fold, P=0.001) and during (6-fold, P<0.0001) treatment as compared with control subjects. Accordingly, serum concentration of IL-6 was also increased by about 50% in thyrotoxic patients as compared with healthy controls (P=0.03). CONCLUSIONS: In Graves' hyperthyroidism regardless of thyroid status, adipose tissue secretion of IL-6, but not of leptin, TNF-alpha or PAI-1, is markedly increased in comparison with euthyroid controls. This suggests that autoimmune thyroidal disorder may regulate adipose tissue release of IL-6.

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