scholarly journals Hyperglycemia in Acute COVID-19 is Characterized by Adipose Tissue Dysfunction and Insulin Resistance

2021 ◽  
Author(s):  
Moritz Reiterer ◽  
Mangala Rajan ◽  
Nicolás Gómez-Banoy ◽  
Jennifer D. Lau ◽  
Luis G. Gomez-Escobar ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Distress Syndrome ◽  
Pancreatic Beta Cell ◽  
Adverse Outcomes ◽  
Pathophysiological Mechanism ◽  
Glucocorticoid Treatment ◽  
Beta Cell Failure ◽  
Adipose Tissue Dysfunction ◽  
Hospital Stays

AbstractCOVID-19 has proven to be a metabolic disease resulting in adverse outcomes in individuals with diabetes or obesity. Patients infected with SARS-CoV-2 and hyperglycemia suffer from longer hospital stays, higher risk of developing acute respiratory distress syndrome (ARDS), and increased mortality compared to those who do not develop hyperglycemia. Nevertheless, the pathophysiological mechanism(s) of hyperglycemia in COVID-19 remains poorly characterized. Here we show that insulin resistance rather than pancreatic beta cell failure is the prevalent cause of hyperglycemia in COVID-19 patients with ARDS, independent of glucocorticoid treatment. A screen of protein hormones that regulate glucose homeostasis reveals that the insulin sensitizing adipokine adiponectin is reduced in hyperglycemic COVID-19 patients. Hamsters infected with SARS-CoV-2 also have diminished expression of adiponectin. Together these data suggest that adipose tissue dysfunction may be a driver of insulin resistance and adverse outcomes in acute COVID-19.

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.

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 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.

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 New opportunities for the correction of non-alcoholic fatty liver disease in men with type 2 diabetes mellitus and hypogonadism

2020 ◽  
Vol 17 (3) ◽  
pp. 241-248
Author(s):  
Irina A. Khripun ◽  
Sergey V. Vorobyev ◽  
Yanina Y. Allahverdieva ◽  
Elizaveta O. Dzantieva ◽  
Maria A. Rasskazova
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Alcoholic Fatty Liver ◽  
Adipose Tissue Dysfunction ◽  
Fat Fraction ◽  
Hypoglycemic Therapy ◽  
Alcoholic Fatty Liver Disease

Background: The common pathogenetic relations of type 2 diabetes mellitus (T2DM), testosterone (T) deficiency and non-alcoholic fatty liver disease (NAFLD) have indicated a new direction in the study of their mutual influence. It was found that NAFLD is more pronounced in men with T2DM and hypogonadism than in eugonadal patients and associated with hyperinsulinemia, insulin resistance, impaired lipid metabolism and adipose tissue dysfunction. However, the effects of testosterone replacement therapy (TRT) on the severity of NAFLD in men with hypogonadism have not been studied.Aims: To study the effect of TRT on the severity of NAFLD in men with T2DM and hypogonadism.MATERIALS AND METHODS: Anthropometric data, biochemical parameters (alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltranspeptidase (GGTP), glucose, immunoreactive insulin, HOMA index, glycosylated hemoglobin, lipidogram), ELISA analysis (total T, LH, sex hormone binding globulin, resistin, adiponectin, leptin), as well as magnetic resonance imaging with determination of the liver fat fraction were examined.Results: The study included 60 men with T2DM and hypogonadism (mean age 54 [49; 57] years), who were randomized into 2 groups: 1 (n=30) - patients who received 1% transdermal T gel (50 mg/day) in addition to standard hypoglycemictherapy; 2 (n=30) - patients who received standard hypoglycemic therapy. The follow-up period was 6 months. T therapy was associated with a decrease in liver enzyme levels: AST by 31%, ALT by 21%, and GGTP by 15.9% (p<0.05) and the hepatic fat fraction by 1.7 times, which reflect the regress of liver inflammation, and, consequently, a decrease in the severity of NAFLD. Moreover, TRT has improved the function of adipose tissue - reduced the concentration of leptin by 1.4 times and resistin by 1.5 times, which was accompanied by an increase in adiponectin level by 1.3 times (p<0.01). The use of TRT was associated with decrease in the severity of visceral obesity, hyperinsulinemia by 1.5 times, an insulin resistance index HOMA by 2.2 times, fasting glycaemia and HbA1c levels, despite constant hypoglycemic therapy. Statistically significant decrease in the levels of total cholesterol and triglycerides was observed in men receiving TRT. Thus, a decrease in adipose tissue dysfunction and insulin resistance in men receiving TRT can be considered as a pathogenetic mechanism responsible for improving liver function and reducing the severity of NAFLD.Conclusions: TRT in men with T2DM and hypogonadism is accompanied by regress of inflammatory activity in liver and intensity of hepatocytes steatosis, reflected by decrease in liver enzymes levels and liver fat fraction.

Sign in / Sign up

Export Citation Format

Share Document