Adipose tissue hypoxia and insulin resistance

2016 ◽  
Vol 64 (4) ◽  
pp. 830-832 ◽  
Author(s):  
Neda Rasouli
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Tissue Hypoxia ◽  
Sequence Of Events ◽  
Adipose Tissue Dysfunction ◽  
Underlying Mechanisms ◽  
Key Events

Despite the well-established association of obesity with insulin resistance and inflammation, the underlying mechanisms and sequence of events leading to inflammation and insulin resistance remain unknown. Adipose tissue hypoxia has been proposed as one of the possible key events during the process of fat expansion that leads to adipose tissue dysfunction. The focus of this paper is reviewing the evidence on adipose tissue hypoxia in obesity and its relation to insulin resistance.

scholarly journals Chronic Intermittent Hypoxia Induces Early-Stage Metabolic Dysfunction Independently of Adipose Tissue Deregulation

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1233
Author(s):  
Fátima O. Martins ◽  
Joana F. Sacramento ◽  
Elena Olea ◽  
Bernardete F. Melo ◽  
Jesus Prieto-Lloret ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Intermittent Hypoxia ◽  
Early Stage ◽  
Tissue Hypoxia ◽  
Whole Body ◽  
Chronic Intermittent Hypoxia ◽  
Adipose Tissue Dysfunction ◽  
Obstructive Sleep

Several studies demonstrated a link between obstructive sleep apnea (OSA) and the development of insulin resistance. However, the main event triggering insulin resistance in OSA remains to be clarified. Herein, we investigated the effect of mild and severe chronic intermittent hypoxia (CIH) on whole-body metabolic deregulation and visceral adipose tissue dysfunction. Moreover, we studied the contribution of obesity to CIH-induced dysmetabolic states. Experiments were performed in male Wistar rats submitted to a control and high-fat (HF) diet. Two CIH protocols were tested: A mild CIH paradigm (5/6 hypoxic (5% O2) cycles/h, 10.5 h/day) during 35 days and a severe CIH paradigm (30 hypoxic (5% O2) cycles, 8 h/day) during 15 days. Fasting glycemia, insulinemia, insulin sensitivity, weight, and fat mass were assessed. Adipose tissue hypoxia, inflammation, angiogenesis, oxidative stress, and metabolism were investigated. Mild and severe CIH increased insulin levels and induced whole-body insulin resistance in control animals, effects not associated with weight gain. In control animals, CIH did not modify adipocytes perimeter as well as adipose tissue hypoxia, angiogenesis, inflammation or oxidative stress. In HF animals, severe CIH attenuated the increase in adipocytes perimeter, adipose tissue hypoxia, angiogenesis, and dysmetabolism. In conclusion, adipose tissue dysfunction is not the main trigger for initial dysmetabolism in CIH. CIH in an early stage might have a protective role against the deleterious effects of HF diet on adipose tissue metabolism.

scholarly journals Drugs Involved in Dyslipidemia and Obesity Treatment: Focus on Adipose Tissue

2018 ◽  
Vol 2018 ◽  
pp. 1-21 ◽  
Author(s):  
Sofia Dias ◽  
Sílvia Paredes ◽  
Laura Ribeiro
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Visceral Obesity ◽  
Atherogenic Dyslipidemia ◽  
Adipose Tissue Dysfunction ◽  
Treatment Focus ◽  
Underlying Mechanisms ◽  
Approved Drugs

Metabolic syndrome can be defined as a state of disturbed metabolic homeostasis characterized by visceral obesity, atherogenic dyslipidemia, arterial hypertension, and insulin resistance. The growing prevalence of metabolic syndrome will certainly contribute to the burden of cardiovascular disease. Obesity and dyslipidemia are main features of metabolic syndrome, and both can present with adipose tissue dysfunction, involved in the pathogenic mechanisms underlying this syndrome. We revised the effects, and underlying mechanisms, of the current approved drugs for dyslipidemia and obesity (fibrates, statins, niacin, resins, ezetimibe, and orlistat; sibutramine; and diethylpropion, phentermine/topiramate, bupropion and naltrexone, and liraglutide) on adipose tissue. Specifically, we explored how these drugs can modulate the complex pathways involved in metabolism, inflammation, atherogenesis, insulin sensitivity, and adipogenesis. The clinical outcomes of adipose tissue modulation by these drugs, as well as differences of major importance for clinical practice between drugs of the same class, were identified. Whether solutions to these issues will be found in further adjustments and combinations between drugs already in use or necessarily in new advances in pharmacology is not known. To better understand the effect of drugs used in dyslipidemia and obesity on adipose tissue not only is challenging for physicians but could also be the next step to tackle cardiovascular disease.

Adipose Tissue Insulin Resistance Is Longitudinally Associated With Adipose Tissue Dysfunction, Circulating Lipids, and Dysglycemia: The PROMISE Cohort

Diabetes Care ◽  
2021 ◽  
pp. dc201918
Author(s):  
Zhila Semnani-Azad ◽  
Philip W. Connelly ◽  
Richard P. Bazinet ◽  
Ravi Retnakaran ◽  
David J. A. Jenkins ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Adipose Tissue Dysfunction

Direct renin inhibition improved insulin resistance and adipose tissue dysfunction in type 2 diabetic KK-Ay mice

2010 ◽  
Vol 28 (7) ◽  
pp. 1471-1481 ◽  
Author(s):  
Masaru Iwai ◽  
Harumi Kanno ◽  
Yumiko Tomono ◽  
Shinji Inaba ◽  
Izumi Senba ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Adipose Tissue Dysfunction ◽  
Renin Inhibition ◽  
Type 2 Diabetic ◽  
Ay Mice

scholarly journals Rab4b Deficiency in T Cells Promotes Adipose Treg/Th17 Imbalance, Adipose Tissue Dysfunction, and Insulin Resistance

Cell Reports ◽  
2018 ◽  
Vol 25 (12) ◽  
pp. 3329-3341.e5 ◽  
Author(s):  
Jérôme Gilleron ◽  
Gwennaëlle Bouget ◽  
Stoyan Ivanov ◽  
Cindy Meziat ◽  
Franck Ceppo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
T Cells ◽  
Adipose Tissue ◽  
Adipose Tissue Dysfunction

scholarly journals Obesity, inflammation, and insulin resistance

2014 ◽  
Vol 50 (4) ◽  
pp. 677-692 ◽  
Author(s):  
Luana Mota Martins ◽  
Ana Raquel Soares Oliveira ◽  
Kyria Jayanne Clímaco Cruz ◽  
Francisco Leonardo Torres-Leal ◽  
Dilina do Nascimento Marreiro
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Biologically Active ◽  
Endocrine Organ ◽  
Adipose Tissue Dysfunction ◽  
Current Review ◽  
Increased Risk ◽  
Anti Inflammatory ◽  
Inflammatory Molecules ◽  
Inflammatory Action

White adipose tissue (WAT) is considered an endocrine organ. When present in excess, WAT can influence metabolism via biologically active molecules. Following unregulated production of such molecules, adipose tissue dysfunction results, contributing to complications associated with obesity. Previous studies have implicated pro- and anti-inflammatory substances in the regulation of inflammatory response and in the development of insulin resistance. In obese individuals, pro-inflammatory molecules produced by adipose tissue contribute to the development of insulin resistance and increased risk of cardiovascular disease. On the other hand, the molecules with anti-inflammatory action, that have been associated with the improvement of insulin sensitivity, have your decreased production. Imbalance of these substances contributes significantly to metabolic disorders found in obese individuals. The current review aims to provide updated information regarding the activity of biomolecules produced by WAT.

scholarly journals Continuous 24-h nicotinic acid infusion in rats causes FFA rebound and insulin resistance by altering gene expression and basal lipolysis in adipose tissue

2011 ◽  
Vol 300 (6) ◽  
pp. E1012-E1021 ◽  
Author(s):  
Young Taek Oh ◽  
Ki-Sook Oh ◽  
Yong Min Choi ◽  
Anne Jokiaho ◽  
Casey Donovan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Nicotinic Acid ◽  
Molecular Mechanisms ◽  
Lipid Lowering ◽  
Plasma Ffa ◽  
Phosphodiesterase 3B ◽  
Altered Gene ◽  
Underlying Mechanisms

Nicotinic acid (NA) has been used as a lipid drug for five decades. The lipid-lowering effects of NA are attributed to its ability to suppress lipolysis in adipocytes and lower plasma FFA levels. However, plasma FFA levels often rebound during NA treatment, offsetting some of the lipid-lowering effects of NA and/or causing insulin resistance, but the underlying mechanisms are unclear. The present study was designed to determine whether a prolonged, continuous NA infusion in rats produces a FFA rebound and/or insulin resistance. NA infusion rapidly lowered plasma FFA levels (>60%, P < 0.01), and this effect was maintained for ≥5 h. However, when this infusion was extended to 24 h, plasma FFA levels rebounded to the levels of saline-infused control rats. This was not due to a downregulation of NA action, because when the NA infusion was stopped, plasma FFA levels rapidly increased more than twofold ( P < 0.01), indicating that basal lipolysis was increased. Microarray analysis revealed many changes in gene expression in adipose tissue, which would contribute to the increase in basal lipolysis. In particular, phosphodiesterase-3B gene expression decreased significantly, which would increase cAMP levels and thus lipolysis. Hyperinsulinemic glucose clamps showed that insulin's action on glucose metabolism was improved during 24-h NA infusion but became impaired with increased plasma FFA levels after cessation of NA infusion. In conclusion, a 24-h continuous NA infusion in rats resulted in an FFA rebound, which appeared to be due to altered gene expression and increased basal lipolysis in adipose tissue. In addition, our data support a previous suggestion that insulin resistance develops as a result of FFA rebound during NA treatment. Thus, the present study provides an animal model and potential molecular mechanisms of FFA rebound and insulin resistance, observed in clinical studies with chronic NA treatment.

scholarly journals Insulin resistance is associated with altered amino acid metabolism and adipose tissue dysfunction in normoglycemic women

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Petri Wiklund ◽  
Xiaobo Zhang ◽  
Satu Pekkala ◽  
Reija Autio ◽  
Lingjia Kong ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Amino Acid ◽  
Amino Acid Metabolism ◽  
Acid Metabolism ◽  
Adipose Tissue Dysfunction

Hyperandrogenism, Insulin Resistance, and Acanthosis Nigricans (HAIR-AN) Syndrome Reflects Adipose Tissue Dysfunction (“Adiposopathy” or “Sick Fat”) in Asian Indian Girls

Dermatology ◽  
2021 ◽  
pp. 1-9
Author(s):  
Kritika Agrawal ◽  
Rachita Mathur ◽  
Naincy Purwar ◽  
Sandeep Kumar Mathur ◽  
Deepak Kumar Mathur
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Inflammatory Markers ◽  
Tertiary Care ◽  
Serum Adiponectin ◽  
Primary Role ◽  
Care Hospital ◽  
Adipose Tissue Dysfunction ◽  
Tnf Α

<b><i>Background:</i></b> Whether HAIR-AN syndrome and polycystic ovarian syndrome (PCOS) are distinct entities or represent a phenotypic spectrum of the same syndrome is still unclear. HAIR-AN syndrome is characterized by high insulin resistance, obesity, and hyperinsulinemia as compared to PCOS and could represent adipose tissue dysfunction as the primary pathophysiologic trigger. This study was undertaken to study the role of adipose tissue dysfunction in HAIR-AN syndrome and PCOS using adipocytokines as surrogate markers of “adiposopathy.” <b><i>Materials and Methods:</i></b> A cross-sectional observational study was conducted at a tertiary care hospital over a period of 1 year. Serum adiponectin, leptin, IL-6, and TNF-α levels were measured in 30 women with HAIR-AN syndrome and in 30 women with PCOS. Correlations between adipocytokines, inflammatory markers, serum testosterone, and serum insulin were determined. Data analysis was performed using the SPSS version 23.0 (IBM SPSS Statistics Inc., Chicago, IL, USA) software program. <b><i>Results:</i></b> Women with HAIR-AN syndrome had significantly higher hyperandrogenemia, hyperinsulinemia, and insulin resistance as compared to PCOS women. They also had high leptin levels and lower adiponectin levels (<i>p</i> &#x3c; 0.001). However, the levels of inflammatory markers (TNF-α and IL-6) were similar in both the groups (<i>p</i> &#x3e; 0.05). Serum adiponectin showed a negative correlation with HOMA-IR and testosterone levels, while leptin showed a positive correlation with both in HAIR-AN patients while no such correlation was found in the PCOS group. <b><i>Conclusion:</i></b> The significantly raised adipocytokines in HAIR-AN syndrome patients as compared to PCOS patients indicates the primary role of adipose tissue dysfunction (“adiposopathy”) in the pathogenesis of HAIR-AN syndrome while only a minor role, if any, in PCOS. Both these syndromes stand as distinct entities pathogenically with an overlapping phenotype.

Sign in / Sign up

Export Citation Format

Share Document