scholarly journals Testicles, adipose organ and heart: a new axis in the management of SARS-CoV-2?

2021 ◽  
pp. 110587
Author(s):  
Alexander Bertuccioli ◽  
Marco Cardinali ◽  
Francesco Di Pierro
Keyword(s):  
Adipose Organ

STUDIES IN CONGENITAL GENERALIZED LIPODYSTROPHY (SEIP-BERARDINELLI SYNDROME)

1973 ◽  
Vol 72 (3) ◽  
pp. 475-494 ◽  
Author(s):  
Svein Oseid
Keyword(s):  
Insulin Resistance ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Juvenile Form ◽  
Congenital Generalized Lipodystrophy ◽  
Glucose Levels ◽  
Normal Glucose ◽  
Glucose Tolerance Tests ◽  
The One ◽  
Adipose Organ

ABSTRACT Six cases of congenital generalized lipodystrophy have been studied at different ages from infancy to adolescence with regard to glucose tolerance, insulin secretion, and insulin sensitivity. During the first few years of life there is normal glucose tolerance. The fasting immuno-reactive insulin (IRI) levels are either slightly elevated or normal. The IRI response to glucose is exaggerated and prolonged, at least from the third year of life. Some degree of insulin resistance is already present in infancy. From the age of 8–10 years glucose tolerance decreases rapidly. The fasting IRI levels are usually grossly elevated, while fasting plasma glucose levels are only moderately elevated or normal. The IRI responses to oral and iv administered glucose, and to tolbutamide are exaggerated; the insulinogenic indices are high. Cortisone primed glucose tolerance tests become abnormal. Insulin resistance is marked, and increases with age. After cessation of growth at approximately 12 years of age, frank diabetes with fasting hyperglycaemia and diabetic glucose tolerance curves developed in the one patient followed beyond this age. Her fasting IRI was increased, but there was a poor IRI response to glucose stimulation, suggesting a partial exhaustion of the β-cells. Her initial IRI response to tolbutamide was still good, but not as brisk as in the younger patients. This type of diabetes is quite different from the juvenile form, and also from the diabetes of older age. It may be causally related to the lack of an adequate adipose organ necessary for the disposal of excesses of glucose, or possibly related to another anti-insulin mechanism.

scholarly journals The Role of Dysfunctional Adipose Tissue in Pancreatic Cancer: A Molecular Perspective

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1849 ◽  
Author(s):  
Davide Brocco ◽  
Rosalba Florio ◽  
Laura De Lellis ◽  
Serena Veschi ◽  
Antonino Grassadonia ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Adipose Tissue ◽  
Molecular Mechanisms ◽  
Normal Weight ◽  
Therapeutic Options ◽  
Therapeutic Interventions ◽  
Fat Accumulation ◽  
Adipose Organ ◽  
The Impact

Pancreatic cancer (PC) is a lethal malignancy with rising incidence and limited therapeutic options. Obesity is a well-established risk factor for PC development. Moreover, it negatively affects outcome in PC patients. Excessive fat accumulation in obese, over- and normal-weight individuals induces metabolic and inflammatory changes of adipose tissue microenvironment leading to a dysfunctional adipose “organ”. This may drive the association between abnormal fat accumulation and pancreatic cancer. In this review, we describe several molecular mechanisms that underpin this association at both local and systemic levels. We focus on the role of adipose tissue-derived circulating factors including adipokines, hormones and pro-inflammatory cytokines, as well as on the impact of the local adipose tissue in promoting PC. A discussion on potential therapeutic interventions, interfering with pro-tumorigenic effects of dysfunctional adipose tissue in PC, is included. Considering the raise of global obesity, research efforts to uncover the molecular basis of the relationship between pancreatic cancer and adipose tissue dysfunction may provide novel insights for the prevention of this deadly disease. In addition, these efforts may uncover novel targets for personalized interventional strategies aimed at improving the currently unsatisfactory PC therapeutic options.

Oxidative stress and lipid peroxidation by-products at the crossroad between adipose organ dysregulation and obesity-linked insulin resistance

Biochimie ◽  
2013 ◽  
Vol 95 (3) ◽  
pp. 585-594 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Marta Piroddi ◽  
Francesca Luchetti ◽  
Cristina Tortoioli ◽  
Barbara Canonico ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Lipid Peroxidation ◽  
Adipose Organ ◽  
By Products

The Adipose Organ: Morphological Perspectives of Adipose Tissues

2014 ◽  
pp. 123-133
Author(s):  
Arianna Smorlesi ◽  
Andrea Frontini ◽  
Saverio Cinti
Keyword(s):  
Adipose Tissues ◽  
Adipose Organ

scholarly journals Assembling the adipose organ: adipocyte lineage segregation and adipogenesisin vivo

Development ◽  
2019 ◽  
Vol 146 (7) ◽  
pp. dev172098 ◽  
Author(s):  
Zachary L. Sebo ◽  
Matthew S. Rodeheffer
Keyword(s):  
Adipose Organ

scholarly journals Severe Brown Fat Lipoatrophy Aggravates Atherosclerotic Process in Male Mice

Endocrinology ◽  
2016 ◽  
Vol 157 (9) ◽  
pp. 3517-3528 ◽  
Author(s):  
Almudena Gómez-Hernández ◽  
Nuria Beneit ◽  
Óscar Escribano ◽  
Sabela Díaz-Castroverde ◽  
Gema García-Gómez ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Vascular Inflammation ◽  
Brown Fat ◽  
Visceral Adiposity ◽  
Perivascular Adipose Tissue ◽  
Metabolic Alterations ◽  
Brown Adipose ◽  
Apo E ◽  
Atherosclerotic Process ◽  
Adipose Organ

Obesity is one of the major risk factors for the development of cardiovascular diseases and is characterized by abnormal accumulation of adipose tissue, including perivascular adipose tissue (PVAT). However, brown adipose tissue (BAT) activation reduces visceral adiposity. To demonstrate that severe brown fat lipoatrophy might accelerate atherosclerotic process, we generated a new mouse model without insulin receptor (IR) in BAT and without apolipoprotein (Apo)E (BAT-specific IR knockout [BATIRKO];ApoE−/− mice) and assessed vascular and metabolic alterations associated to obesity. In addition, we analyzed the contribution of the adipose organ to vascular inflammation. Brown fat lipoatrophy induces visceral adiposity, mainly in gonadal depot (gonadal white adipose tissue [gWAT]), severe glucose intolerance, high postprandial glucose levels, and a severe defect in acute insulin secretion. BATIRKO;ApoE−/− mice showed greater hypertriglyceridemia than the obtained in ApoE−/− and hypercholesterolemia similar to ApoE−/− mice. BATIRKO;ApoE−/− mice, in addition to primary insulin resistance in BAT, also showed a significant decrease in insulin signaling in liver, gWAT, heart, aorta artery, and thoracic PVAT. More importantly, our results suggest that severe brown fat lipoatrophy aggravates the atherosclerotic process, characterized by a significant increase of lipid depots, atherosclerotic coverage, lesion size and complexity, increased macrophage infiltration, and proinflammatory markers expression. Finally, an increase of TNF-α and leptin as well as a decrease of adiponectin by BAT, gWAT, and thoracic PVAT might also be responsible of vascular damage. Our results suggest that severe brown lipoatrophy aggravates atherosclerotic process. Thus, BAT activation might protect against obesity and its associated metabolic alterations.

scholarly journals Monocyte Chemoattractant Protein-1 in Subcutaneous Abdominal Adipose Tissue: Characterization of Interstitial Concentration and Regulation of Gene Expression by Insulin

2007 ◽  
Vol 92 (7) ◽  
pp. 2688-2695 ◽  
Author(s):  
Giuseppe Murdolo ◽  
Ann Hammarstedt ◽  
Madeléne Sandqvist ◽  
Martin Schmelz ◽  
Christian Herder ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Regulation Of Gene Expression ◽  
Whole Body ◽  
Mrna Levels ◽  
Abdominal Adipose Tissue ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Adipose Organ

Abstract Context: The chemokine monocyte chemoattractant protein-1 (MCP-1) is implicated in obesity-associated chronic inflammation, insulin resistance, and atherosclerosis. Objectives: The objectives of this study were to: 1) characterize the interstitial levels and the gene expression of MCP-1 in the sc abdominal adipose tissue (SCAAT), 2) elucidate the response of MCP-1 to acute hyperinsulinemia, and 3) determine the relationship between MCP-1 and arterial stiffness. Design: Nine lean (L) and nine uncomplicated obese (OB) males were studied in the fasting state and during a euglycemic-hyperinsulinemic clamp combined with the microdialysis technique. Interstitial and serum MCP-1 (iMCP-1 and sMCP-1, respectively) levels, pulse wave analysis, and SCAAT biopsies were characterized at baseline and after hyperinsulinemia. Results: OB showed elevated sMCP-1 (P < 0.01) but similar iMCP-1 levels as compared with L. Basal iMCP-1 concentrations were considerably higher than sMCP-1 (P < 0.0001), and a gradient between iMCP-1 and sMCP-1 levels was maintained throughout the hyperinsulinemia. At baseline, SCAAT gene expression profile revealed a “co-upregulation” of MCP-1, MCP-2, macrophage inflammatory protein-1α, and CD68 in OB, and whole-body glucose disposal inversely correlated with the MCP-1 gene expression. After hyperinsulinemia, MCP-1 and MCP-2 mRNA levels significantly increased in L, but not in OB. Finally, sMCP-1 excess in the OB positively correlated with the stiffer vasculature. Conclusions: These observations demonstrate similar interstitial concentrations and a differential gene response to hyperinsulinemia of MCP-1 in the SCAAT from L and OB individuals. In human obesity, we suggest the SCAAT MCP-1 gene overexpression as a biomarker of an “inflamed” adipose organ and impaired glucose metabolism.

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