scholarly journals Adipocyte differentiation impairment as well as lipid metabolism and transport problems – major causes of genetic lipodystrophies

2019 ◽  
Vol 73 ◽  
pp. 741-761
Author(s):  
Agnieszka Dettlaff-Pokora
Keyword(s):  
Adipose Tissue ◽  
Primary Care Physicians ◽  
Adipocyte Differentiation ◽  
Plasma Cholesterol ◽  
Correct Diagnosis ◽  
Hdl Cholesterol ◽  
Diagnostic Methods ◽  
Tissue Loss ◽  
Ectopic Fat ◽  
Fat Accumulation

Lipodystrophies are heterogenic group of adipose tissue disorders with its general or partial atrophy. In case of congenital lipodystrophies disturbances of adipogenesis or/and alterations of adipocyte differentiation often occur leading to thermogenic adipocytes formation. Basic adipocyte functions can be perturbed, including improper synthesis of triacylglycerols and phospholipids of lipid droplet, but also impaired fatty acids release and intracellular lipid traffic. Lipodystrophy can result from weakening of adipose tissue structure, but also from improper function of both cytoskeleton and nuclear lamina leading to cell dysfunction. Lack of adipose tissue leads to a) increased plasma triacylglycerols level and ectopic fat accumulation in other tissues; b) total plasma cholesterol increase; c) plasma HDL-cholesterol decrease. Ectopic fat accumulation in liver can cause fatty liver and with time can lead to hepatomegaly and liver cirrhosis. Dysfunctions are proportional to the extent of fat tissue loss with generalized lipodystrophies patients developing complications at early ages. Diabetes and insulin resistance are common comorbidities. Improvement of diagnostic methods of medical genetics allows precise determination of their genotypes and correct diagnosis of patients suffering from lipodystrophy. For that reason number of described cases increased in recent years, also in Poland. New lipodystrophy types were described. Therefore there is a need to bring lipodystrophy syndromes for the attention of primary care physicians, pediatricians and endocrinologists.

scholarly journals Adipocytedifferentiationimpairment as well as lipid metabolism and trasportproblems – major causes of geneticlipodystrophies

2019 ◽  
Vol 73 ◽  
pp. 1-39
Author(s):  
Agnieszka Dettlaff-Pokora
Keyword(s):  
Adipose Tissue ◽  
Primary Care Physicians ◽  
Plasma Cholesterol ◽  
Correct Diagnosis ◽  
Hdl Cholesterol ◽  
Precise Determination ◽  
Diagnostic Methods ◽  
Tissue Loss ◽  
Ectopic Fat ◽  
Fat Accumulation

Lipodystrophies are heterogenic group of adipose tissue disorders with its general or partial atrophy. In case of congenital lipodystrophies disturbances of adipogenesis or/and alterations of adipocyte differentiation often occur leading to thermogenic adipocytes formation. Basic adipocyte functions can be perturbed, including improper synthesis of triacylglycerols and phospholipids of lipid droplet, but also impaired fatty acids release and intracellular lipid traffic. Lipodystrophy can result from weakening of adipose tissue structure, but also from improper function of both cytoskeleton and nuclear lamina leading to cell dysfunction. Lack of adipose tissue leads to a) increased plasma triacylglycerols level and ectopic fat accumulation in other tissues; b) total plasma cholesterol increase; c) plasma HDL-cholesterol decrease. Ectopic fat accumulation in liver can cause fatty liver and with time can lead to hepatomegaly and liver cirrhosis. Dysfunctionsare proportional to the extent of fat tissue loss with generalized lipodystrophies patients developing complications at early ages. Diabetes and insulin resistance are common comorbidities. Improvement of diagnostic methods of medical genetics allows precise determination of their genotypes and correct diagnosis of patients suffering from lipodystrophy. For that reason number of described cases increased in recent years, also in Poland. New lipodystrophy types were described. Therefore there is a need to bring lipodystrophy syndromes for the attention of primary care physicians, pediatricians and endocrinologists.

scholarly journals The Relationships of Plasma Adiponectin with a Favorable Lipid Profile, Decreased Inflammation, and Less Ectopic Fat Accumulation Depend on Adiposity

2006 ◽  
Vol 52 (10) ◽  
pp. 1934-1942 ◽  
Author(s):  
Konstantinos Kantartzis ◽  
Killian Rittig ◽  
Bernd Balletshofer ◽  
Jürgen Machann ◽  
Fritz Schick ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Endothelial Function ◽  
Visceral Adipose Tissue ◽  
Hdl Cholesterol ◽  
Ectopic Fat ◽  
Fat Accumulation ◽  
Plasma Adiponectin ◽  
Markers Of Inflammation ◽  
Visceral Adipose ◽  
The Relationship

Abstract Background: The metabolic effects of adiponectin, including insulin sensitivity, seem to become stronger with increasing adiposity. Adiposity may also affect the relationship of adiponectin concentrations with serum lipid profile; markers of inflammation, atherosclerosis, and endothelial function; and ectopic fat accumulation. Methods: We measured plasma adiponectin concentrations, serum lipids, and serum markers of inflammation, atherosclerosis, and endothelial function in 242 Caucasians without type 2 diabetes. We also measured visceral adipose tissue with magnetic resonance tomography and liver and intramyocellular fat with 1H magnetic resonance spectroscopy. Results: We divided the study participants into 2 groups: lean [mean (SE) total body fat, 26% (0.6%); n = 119] and obese [36% (0.6%); n = 123]. In the obese group, plasma adiponectin concentrations showed a strong positive association with concentrations of HDL cholesterol (P <0.0001) and negative associations with LDL cholesterol, triglycerides, high-sensitivity C-reactive protein, interleukin 6, apolipoprotein B100, soluble E-selectin, soluble vascular cellular adhesion molecule 1, plasminogen activator inhibitor 1, leukocyte count, and liver and intramyocellular fat (all P <0.03). In the lean group, adiponectin showed a less strong association with HDL cholesterol (P = 0.005) and liver fat (P = 0.03) and no significant associations with the other variables (all P >0.10). High visceral adipose tissue was a strong predictor of low adiponectin concentrations, particularly in the obese group, and attenuated many of the significant relationships. Conclusions: High adiponectin plasma concentrations are associated with favorable lipid profiles, decreased subclinical inflammation, decreased markers of atherosclerosis and endothelial function, and low ectopic fat accumulation, particularly in obese persons. Adiponectin may also have a concentration-related effect on the relationship between visceral adipose tissue and these metabolic characteristics, especially in obese persons.

scholarly journals Obesity and Fat Metabolism in Human Immunodeficiency Virus–Infected Individuals: Immunopathogenic Mechanisms and Clinical Implications

2019 ◽  
Vol 220 (3) ◽  
pp. 420-431 ◽  
Author(s):  
Catherine Godfrey ◽  
Andrew Bremer ◽  
Diana Alba ◽  
Caroline Apovian ◽  
John R Koethe ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Adipose Tissue ◽  
Immune Cell ◽  
Clinical Care ◽  
Fat Metabolism ◽  
Visceral Obesity ◽  
Ectopic Fat ◽  
Metabolic Complications ◽  
Fat Accumulation ◽  
Immunodeficiency Virus

Abstract Metabolic complications relating to complex effects of viral and immune-mediated mechanisms are now a focus of clinical care among persons living with human immunodeficiency virus (PLHIV), and obesity is emerging as a critical problem. To address knowledge gaps, the US National Institutes of Health sponsored a symposium in May 2018 entitled “Obesity and Fat Metabolism in HIV-infected Individuals.” Mechanisms relating to adipose dysfunction and fibrosis, immune function, inflammation, and gastrointestinal integrity were highlighted as contributors to obesity among PLHIV. Fibrotic subcutaneous adipose tissue is metabolically dysfunctional and loses its capacity to expand, leading to fat redistribution, including visceral obesity and ectopic fat accumulation, promoting insulin resistance. Viral proteins, including viral protein R and negative regulatory factor, have effects on adipogenic pathways and cellular metabolism in resident macrophages and T cells. HIV also affects immune cell trafficking into the adipose compartments, with effects on adipogenesis, lipolysis, and ectopic fat accumulation. Key cellular metabolic functions are likely to be affected in PLHIV by gut-derived cytokines and altered microbiota. There are limited strategies to reduce obesity specifically in PLHIV. Enhancing our understanding of critical pathogenic mechanisms will enable the development of novel therapeutics that may normalize adipose tissue function and distribution, reduce inflammation, and improve insulin sensitivity in PLHIV.

scholarly journals Expression profiling of 11β-hydroxysteroid dehydrogenase type-1 and glucocorticoid-target genes in subcutaneous and omental human preadipocytes

2006 ◽  
Vol 37 (2) ◽  
pp. 327-340 ◽  
Author(s):  
I J Bujalska ◽  
M Quinkler ◽  
J W Tomlinson ◽  
C T Montague ◽  
D M Smith ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Target Genes ◽  
Adipocyte Differentiation ◽  
Human Adipose Tissue ◽  
Fat Accumulation ◽  
Visceral Fat Accumulation ◽  
Human Preadipocytes ◽  
Upregulated Genes ◽  
Microarray Technique

Obesity is associated with increased morbidity and mortality from cardiovascular disease, diabetes and cancer. Although obesity is a multi-factorial heterogeneous condition, fat accumulation in visceral depots is most highly associated with these risks. Pathological glucocorticoid excess (i.e. in Cushing’s syndrome) is a recognised, reversible cause of visceral fat accumulation. The aim of this study was to identify depot-specific glucocorticoid-target genes in adipocyte precursor cells (preadipocytes) using Affymetrix microarray technique. Confluent preadipocytes from subcutaneous (SC) and omental (OM) adipose tissue collected from five female patients were treated for 24 h with 100 nM cortisol (F), RNA was pooled and hybridised to the Affymetrix U133 microarray set. We identified 72 upregulated and 30 downregulated genes by F in SC cells. In OM preadipocytes, 56 genes were increased and 19 were decreased. Among the most interesting were transcription factors, markers of adipocyte differentiation and glucose metabolism, cell adhesion and growth arrest protein factors involved in G-coupled and Wnt signalling. The Affymetrix data have been confirmed by quantitative real-time PCR for ten specific genes, including HSD11B1, GR, C/EBPα, C/EBPβ, IL-6, FABP4, APOD, IRS2, AGTR1 and GHR. One of the most upregulated genes in OM but not in SC cells was HSD11B1. The GR was similarly expressed and not regulated by glucocorticoids in SC and OM human preadipocytes. C/EBPα was expressed in SC preadipocytes and upregulated by F, but was below the detection level in OM cells. C/EBPβ was highly expressed both in SC and in OM preadipocytes, but was not regulated by F. Our results provide insight into the genes involved in the regulation of adipocyte differentiation by cortisol, highlighting the depot specifically in human adipose tissue.

Phenotypical heterogeneity linked to adipose tissue dysfunction in patients with Type 2 diabetes

2016 ◽  
Vol 130 (19) ◽  
pp. 1753-1762 ◽  
Author(s):  
Ilaria Barchetta ◽  
Francesco Angelico ◽  
Maria Del Ben ◽  
Michele Di Martino ◽  
Flavia Agata Cimini ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Insulin Secretion ◽  
Fat Deposition ◽  
Metabolic Phenotype ◽  
Ectopic Fat ◽  
Model Assessment ◽  
Fat Accumulation

Adipose tissue (AT) inflammation leads to increased free fatty acid (FFA) efflux and ectopic fat deposition, but whether AT dysfunction drives selective fat accumulation in specific sites remains unknown. The aim of the present study was to investigate the correlation between AT dysfunction, hepatic/pancreatic fat fraction (HFF, PFF) and the associated metabolic phenotype in patients with Type 2 diabetes (T2D). Sixty-five consecutive T2D patients were recruited at the Diabetes Centre of Sapienza University, Rome, Italy. The study population underwent clinical examination and blood sampling for routine biochemistry and calculation of insulin secretion [homoeostasis model assessment of insulin secretion (HOMA-β%)] and insulin-resistance [homoeostasis model assessment of insulin resistance (HOMA-IR) and adipose tissue insulin resistance (ADIPO-IR)] indexes. Subcutaneous (SAT) and visceral (VAT) AT area, HFF and PFF were determined by magnetic resonance. Some 55.4% of T2D patients had non-alcoholic fatty liver disease (NAFLD); they were significantly younger and more insulin-resistant than non-NAFLD subjects. ADIPO-IR was the main determinant of HFF independently of age, sex, HOMA-IR, VAT, SAT and predicted severe NAFLD with the area under the receiver operating characteristic curve (AUROC)=0.796 (95% confidence interval: 0.65–0.94, P=0.001). PFF was independently associated with increased total adiposity but did not correlate with AT dysfunction, insulin resistance and secretion or NAFLD. The ADIPO-IR index was capable of predicting NAFLD independently of all confounders, whereas it did not seem to be related to intrapancreatic fat deposition; unlike HFF, higher PFF was not associated with relevant alterations in the metabolic profile. In conclusion, the presence and severity of AT dysfunction may drive ectopic fat accumulation towards specific targets, such as VAT and liver, therefore evaluation of AT dysfunction may contribute to the identification of different risk profiles among T2D patients.

1866-P: Peripancreatic Adipose Tissue Protects against Ectopic Fat Accumulation in the Liver

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1866-P
Author(s):  
BELÉN CHANCLÓN ◽  
PETER MICALLEF ◽  
ELIN BANKE NORDBECK ◽  
YANLING WU ◽  
BJÖRN WILDER ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Ectopic Fat ◽  
Fat Accumulation

scholarly journals Hypertrophic Obesity and Subcutaneous Adipose Tissue Dysfunction

2014 ◽  
Vol 6 (2) ◽  
pp. 79
Author(s):  
Anna Meiliana ◽  
Andi Wijaya
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Ectopic Fat ◽  
Metabolic Complications ◽  
Fat Accumulation ◽  
Insulin Resistant ◽  
Fat Redistribution ◽  
Subcutaneous Adipose

BACKGROUND: Over the past 50 years, scientists have recognized that not all adipose tissue is alike, and that health risk is associated with the location as well as the amount of body fat. Different depots are sufficiently distinct with respect to fatty-acid storage and release as to probably play unique roles in human physiology. Whether fat redistribution causes metabolic disease or whether it is a marker of underlying processes that are primarily responsible is an open question.CONTENT: The limited expandability of the subcutaneous adipose tissue leads to inappropriate adipose cell expansion (hypertrophic obesity) with local inflammation and a dysregulated and insulin-resistant adipose tissue. The inability to store excess fat in the subcutaneous adipose tissue is a likely key mechanism for promoting ectopic fat accumulation in tissues and areas where fat can be stored, including the intra-abdominal and visceral areas, in the liver, epi/pericardial area, around vessels, in the myocardium, and in the skeletal muscles. Many studies have implicated ectopic fat accumulation and the associated lipotoxicity as the major determinant of the metabolic complications of obesity driving systemic insulin resistance, inflammation, hepatic glucose production, and dyslipidemia.SUMMARY: In summary, hypertrophic obesity is due to an impaired ability to recruit and differentiate available adipose precursor cells in the subcutaneous adipose tissue. Thus, the subcutaneous adipose tissue may be particular in its limited ability in certain individuals to undergo adipogenesis during weight increase. Inability to promote subcutaneous adipogenesis under periods of affluence would favor lipid overlow and ectopic fat accumulation with negative metabolic consequences.KEYWORDS: obesity, adipogenesis, subcutaneous adipose tissue, visceral adipose tissue, adipocyte dysfunction

Beneficial effects of carrots (Daucus carota) on adipocyte differentiation, glucose uptake, and fat accumulation

Planta Medica ◽  
2010 ◽  
Vol 76 (12) ◽  
Author(s):  
K Christensen ◽  
D Kotowska ◽  
L Olsen ◽  
S Bhattacharya ◽  
X Fretté ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Daucus Carota ◽  
Adipocyte Differentiation ◽  
Fat Accumulation ◽  
Beneficial Effects

The Effect of n-3 Fatty Acids on Lipids and Haemostasis in Patients with Type lla and Type IV Hyperlipidaemia

1989 ◽  
Vol 62 (02) ◽  
pp. 797-801 ◽  
Author(s):  
E Berg Schmidt ◽  
E Ernst ◽  
K Varming ◽  
J O Pedersen ◽  
J Dyerberg
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Plasma Cholesterol ◽  
Hdl Cholesterol ◽  
Apolipoprotein A1 ◽  
Type Iv ◽  
Before And After ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Antigen

SummaryPlasma lipids and haemostasis were investigated in 17 patients with hyperlipidaemia before and after 6 weeks supplementation with 6 g n-3 fatty acids. Nine of the patients had type IIa and 8 had type IV hyperlipidaemia. No effect on plasma cholesterol, LDL- or HDL-cholesterol were seen, but plasma triglycerides decreased after n-3 supplementation. Apolipoprotein B increased and apolipoprotein A1 decreased after the oil supplement. The bleeding time was prolonged, but platelet aggregation was unaltered by n-3 fatty acids. Protein C activity increased in type II a and decreased in type IV after the supplement. Fibrinolysis was markedly depressed while von Willebrand factor antigen was reduced after intake of n-3 fatty acids.

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