scholarly journals Selective Impairment of Glucose but Not Fatty Acid or Oxidative Metabolism in Brown Adipose Tissue of Subjects With Type 2 Diabetes

Diabetes ◽  
2015 ◽  
Vol 64 (7) ◽  
pp. 2388-2397 ◽  
Author(s):  
Denis P. Blondin ◽  
Sébastien M. Labbé ◽  
Christophe Noll ◽  
Margaret Kunach ◽  
Serge Phoenix ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Oxidative Metabolism ◽  
Brown Adipose ◽  
Selective Impairment

scholarly journals Rosiglitazone-induced changes in the oxidative stress metabolism and fatty acid composition in relation with trace element status in the primary adipocytes

2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Duygu Aydemir ◽  
Ehsan Sarayloo ◽  
Nuriye Nuray Ulusu
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Trace Element ◽  
Acid Composition ◽  
Brown Adipose

Summary Background Metabolic syndrome, obesity and type 2 diabetes are metabolic disorders characterized by the insulin resistance and the impairment in the insulin secretion. Since impairment in the oxidative stress and adipocyte metabolism contribute to the formation of obesity and diabetes, targeting adipose tissue can be considered as an effective approach to fight against them. Rosiglitazone is used for treatment for patients with type 2 diabetes via inducing lipogenesis and transdifferentiation of white adipose tissue into brown adipose tissue. Since the development of such therapeutics is required to control the formation and function of brown fat cells, we aimed to reveal possible molecular mechanisms behind rosiglitazone induced biochemical changes in the adipose tissue. Methods Cells were expanded in the adipocyte culture medium supplemented with 5 μg/mL insulin following 2 days’ induction. After those cells were treated with rosiglitazone 0, 0.1 3 mol/L and 10 μmol/L rosiglitazone for 48 hours and at 8th day, cells were collected and stored at -80 °C. Then the cells were used to evaluate antioxidant enzyme activities, mineral and trace element levels and fatty acid composition. Results Glucose-6-phosphate dehydrogenase and glutathione reductase significantly reduced in rosiglitazone-treated groups compared to the control. Na, Mg, K, Ca, Cr, Fe, Ni, Cu, Zn, Rb, Sr, Cs, Ba and Pb were determined in the cell lysates via ICP-MS. Also, relative FAME content decreased in the rosiglitazone-treated groups compared to the control. Conclusions Rosiglitazone treatment at low doses showed promising results which may promote brown adipose tissue formation.

scholarly journals Melatonin Enhances the Mitochondrial Functionality of Brown Adipose Tissue in Obese—Diabetic Rats

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1482
Author(s):  
Ahmad Agil ◽  
Miguel Navarro-Alarcon ◽  
Fatma Abo Zakaib Ali ◽  
Ashraf Albrakati ◽  
Diego Salagre ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Superoxide Dismutase ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Superoxide Dismutase Activity ◽  
Atp Production ◽  
Brown Adipose ◽  
Zdf Rats

Developing novel drugs/targets remains a major effort toward controlling obesity-related type 2 diabetes (diabesity). Melatonin controls obesity and improves glucose homeostasis in rodents, mainly via the thermogenic effects of increasing the amount of brown adipose tissue (BAT) and increases in mitochondrial mass, amount of UCP1 protein, and thermogenic capacity. Importantly, mitochondria are widely known as a therapeutic target of melatonin; however, direct evidence of melatonin on the function of mitochondria from BAT and the mechanistic pathways underlying these effects remains lacking. This study investigated the effects of melatonin on mitochondrial functions in BAT of Zücker diabetic fatty (ZDF) rats, which are considered a model of obesity-related type 2 diabetes mellitus (T2DM). At five weeks of age, Zücker lean (ZL) and ZDF rats were subdivided into two groups, consisting of control and treated with oral melatonin for six weeks. Mitochondria were isolated from BAT of animals from both groups, using subcellular fractionation techniques, followed by measurement of several mitochondrial parameters, including respiratory control ratio (RCR), phosphorylation coefficient (ADP/O ratio), ATP production, level of mitochondrial nitrites, superoxide dismutase activity, and alteration in the mitochondrial permeability transition pore (mPTP). Interestingly, melatonin increased RCR in mitochondria from brown fat of both ZL and ZDF rats through the reduction of the proton leak component of respiration (state 4). In addition, melatonin improved the ADP/O ratio in obese rats and augmented ATP production in lean rats. Further, melatonin reduced mitochondrial nitrosative and oxidative status by decreasing nitrite levels and increasing superoxide dismutase activity in both groups, as well as inhibited mPTP in mitochondria isolated from brown fat. Taken together, the present data revealed that chronic oral administration of melatonin improved mitochondrial respiration in brown adipocytes, while decreasing oxidative and nitrosative stress and susceptibility of adipocytes to apoptosis in ZDF rats, suggesting a beneficial use in the treatment of diabesity. Further research regarding the molecular mechanisms underlying the effects of melatonin on diabesity is warranted.

Brown adipose tissue, thermogenesis, angiogenesis: pathophysiological aspects

2014 ◽  
Vol 19 (1) ◽  
Author(s):  
Jennifer Honek ◽  
Sharon Lim ◽  
Carina Fischer ◽  
Hideki Iwamoto ◽  
Takahiro Seki ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Causes Of Death ◽  
Brown Adipose ◽  
Common Causes ◽  
Brown Adipose Tissue Thermogenesis ◽  
Thermogenic Capacity

AbstractThe number of obese and overweight individuals is globally rising, and obesity-associated disorders such as type 2 diabetes, cardiovascular disease and certain types of cancer are among the most common causes of death. While white adipose tissue is the key player in the storage of energy, active brown adipose tissue expends energy due to its thermogenic capacity. Expanding and activating brown adipose tissue using pharmacological approaches therefore might offer an attractive possibility for therapeutic intervention to counteract obesity and its consequences for metabolic health.

scholarly journals Cold and Exercise: Therapeutic Tools to Activate Brown Adipose Tissue and Combat Obesity

Biology ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 9 ◽  
Author(s):  
Carmem Peres Valgas da Silva ◽  
Diego Hernández-Saavedra ◽  
Joseph White ◽  
Kristin Stanford
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Lipid Uptake ◽  
Mitochondrial Uncoupling ◽  
Bat Activity ◽  
Brown Adipose

The rise in obesity over the last several decades has reached pandemic proportions. Brown adipose tissue (BAT) is a thermogenic organ that is involved in energy expenditure and represents an attractive target to combat both obesity and type 2 diabetes. Cold exposure and exercise training are two stimuli that have been investigated with respect to BAT activation, metabolism, and the contribution of BAT to metabolic health. These two stimuli are of great interest because they have both disparate and converging effects on BAT activation and metabolism. Cold exposure is an effective mechanism to stimulate BAT activity and increase glucose and lipid uptake through mitochondrial uncoupling, resulting in metabolic benefits including elevated energy expenditure and increased insulin sensitivity. Exercise is a therapeutic tool that has marked benefits on systemic metabolism and affects several tissues, including BAT. Compared to cold exposure, studies focused on BAT metabolism and exercise display conflicting results; the majority of studies in rodents and humans demonstrate a reduction in BAT activity and reduced glucose and lipid uptake and storage. In addition to investigations of energy uptake and utilization, recent studies have focused on the effects of cold exposure and exercise on the structural lipids in BAT and secreted factors released from BAT, termed batokines. Cold exposure and exercise induce opposite responses in terms of structural lipids, but an important overlap exists between the effects of cold and exercise on batokines. In this review, we will discuss the similarities and differences of cold exposure and exercise in relation to their effects on BAT activity and metabolism and its relevance for the prevention of obesity and the development of type 2 diabetes.

Liraglutide decreases energy expenditure and does not affect the fat fraction of supraclavicular brown adipose tissue in patients with type 2 diabetes

2020 ◽  
Vol 30 (4) ◽  
pp. 616-624 ◽  
Author(s):  
Huub J. van Eyk ◽  
Elisabeth H.M. Paiman ◽  
Maurice B. Bizino ◽  
Suzanne L. IJzermans ◽  
Fleur Kleiburg ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Brown Adipose ◽  
Fat Fraction

Human Brown Adipose Tissue Density Assessed by Near-Infrared Time-Resolved Spectroscopy Inversely Correlates with the Body Mass Index in Patients with Type 2 Diabetes

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2080-P
Author(s):  
HIRONORI WAKI ◽  
NAOKO WATANABE ◽  
SAYURI FUSE ◽  
YUKO KUROSAWA ◽  
TOSHIMASA YAMAUCHI ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Body Mass Index ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Body Mass ◽  
Near Infrared ◽  
The Body ◽  
Time Resolved ◽  
Brown Adipose
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