scholarly journals Dercum’s Disease: A Case Report of a Patient Having Both Type 1 and Type 2 Dercum’s Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Cameron Moattari ◽  
Richard A. Giovane ◽  
Stephanie DiGiovanni Kinsely
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Tissue ◽  
Standard Of Care ◽  
Endocrine Disorder ◽  
Adiposis Dolorosa ◽  
Management Regimes ◽  
Dercum’S Disease ◽  
Disorder Treatment

Dercum’s disease, or adiposis dolorosa, is a rare disorder which consists of multiple, painful lipomas within the subcutaneous tissue and has a distribution mainly in the abdomen and extremities. Dercum’s disease can be defined as in combination with chronic painful adipose tissue. Although the etiology of Dercum’s disease is not clear, it is thought to be a combination of a neurological and endocrine disorder. Treatment for this disease is centered at managing pain. Although there is no standard of care for managing pain, there are different pain management regimes that are promising.

Reduction of Insulin Signaling Upregulates Angiopoietin-like Protein 4 Through Elevated Free Fatty Acids in Diabetic Mice

2011 ◽  
Vol 120 (03) ◽  
pp. 139-144 ◽  
Author(s):  
N. Mizutani ◽  
N. Ozaki ◽  
Y. Seino ◽  
A. Fukami ◽  
E. Sakamoto ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
High Fat Diet ◽  
Serum Triglyceride ◽  
Diabetic Mice ◽  
Brown Adipose

AbstractAngiopoietin-like protein 4 (Angptl4) is thought to cause an increase in serum triglyceride levels. In the present study, we elucidated Angptl4 expression in the mouse models of type 1 and type 2 diabetes mellitus, and investigated the possible mechanisms involved.Type 1 diabetes was induced in C57BL/6 J mice by treating them with streptozotocin (STZ). Type 2 diabetes was induced by feeding the mice a high-fat diet (HFD) for 18 weeks.The levels of Angptl4 mRNA expression in liver, white adipose tissue (WAT), and brown adipose tissue (BAT) were found to increase in the STZ diabetic mice relative to control mice. This effect was attenuated by insulin administration. In the HFD diabetic mice, the Angptl4 mRNA expression levels were increased in liver, WAT, and BAT. Treatment with metformin for 4 weeks attenuated the increased levels of Angptl4 mRNA. Fatty acids (FAs) such as palmitate and linoleate induced Angptl4 mRNA expression in H4IIE hepatoma cells and 3T3-L1 adipocytes. Treatment with insulin but not metformin attenuated FA-induced Angptl4 mRNA expression in H4IIE. Both insulin and metformin did not influence the effect of FAs in 3T3-L1 cells.These observations demonstrated that Angptl4 mRNA expression was increased through the elevated free FAs in diabetic mice.

Inhibition of Type 1 Iodothyronine Deiodinase by Bisphenol A

2019 ◽  
Vol 51 (10) ◽  
pp. 671-677 ◽  
Author(s):  
Maurício Martins da Silva ◽  
Carlos Frederico Lima Gonçalves ◽  
Leandro Miranda-Alves ◽  
Rodrigo Soares Fortunato ◽  
Denise P. Carvalho ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Bisphenol A ◽  
Brown Adipose Tissue ◽  
Tissue Type ◽  
Deiodinase Activity ◽  
Brown Adipose

AbstractPlastics are ubiquitously present in our daily life and some components of plastics are endocrine-disrupting chemicals, such as bisphenol A and phthalates. Herein, we aimed to evaluate the effect of plastic endocrine disruptors on type 1 and type 2 deiodinase activities, enzymes responsible for the conversion of the pro-hormone T4 into the biologically active thyroid hormone T3, both in vitro and in vivo. Initially, we incubated rat liver type 1 deiodinase and brown adipose tissue type 2 deiodinase samples with 0.5 mM of the plasticizers, and the deiodinase activity was measured. Among them, only BPA was capable to inhibit both type 1 and type 2 deiodinases. Then, adult male Wistar rats were treated orally with bisphenol A (40 mg/kg b.w.) for 15 days and hepatic type 1 deiodinase and brown adipose tissue type 2 deiodinase activities and serum thyroid hormone concentrations were measured. In vivo bisphenol A treatment significantly reduced hepatic type 1 deiodinase activity but did not affect brown adipose tissue type 2 deiodinase activity. Serum T4 levels were higher in bisphenol A group, while T3 remained unchanged. T3/T4 ratio was decreased in rats treated with bisphenol A, reinforcing the idea that peripheral metabolism of thyroid hormone was affected by bisphenol A exposure. Therefore, our results suggest that bisphenol A can affect the metabolism of thyroid hormone thus disrupting thyroid signaling.

scholarly journals Empowerment in the Treatment of Diabetes and Obesity

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Włodzimierz Łuczyński ◽  
Barbara Głowińska-Olszewska ◽  
Artur Bossowski
Keyword(s):  
Standard Of Care ◽  
Patients With Diabetes ◽  
Treatment Of Diabetes ◽  
Based Medicine ◽  
Diabetes And Obesity ◽  
Positive Effect

As the available therapies for diabetes and obesity are not effective enough, diabetologists and educators search for new methods to collaborate with patients in order to support their health behaviors. The aim of this review is to discuss perspectives for the development of new empowerment-type therapies in the treatment of diabetes/obesity. Empowerment is a process whereby patients gain the necessary knowledge to influence their own behavior to improve the quality of their lives. It is carried out in five stages: (1) identify the problem, (2) explain the feelings and meanings, (3) build a plan, (4) act, and (5) experience and assess the execution. Although many years have passed since the advent and popularization of the concept of empowerment, the area remains controversial, mainly with regard to the methodology of therapy. Some previous studies have confirmed the positive effect of empowerment on body weight, metabolic control, and quality of life of patients with type 2 diabetes; however, few studies have been conducted in patients with type 1 diabetes. There is still a need to confirm the effectiveness of empowerment in accordance with Evidence Based Medicine by performing long-term observational studies in a large group of patients. In future, empowerment may become part of the standard of care for patients with diabetes and/or obesity.

scholarly journals Polarização de macrófagos e as complicações da Obesidade: o que podemos aprender com os modelos experimentais

2016 ◽  
Vol 95 (2) ◽  
pp. 103
Author(s):  
Brendha Cação ◽  
Ávaro Simões ◽  
Cícero Mendes ◽  
Heraldo P. Souza
Keyword(s):  
Adipose Tissue ◽  
Macrophage Polarization ◽  
Experimental Studies ◽  
Experimental Models ◽  
Lifestyle Changes ◽  
Pubmed Database ◽  
Open Question

Clinical and experimental evidences pointed to the role of immune cells and inflammatory mediators on the development of diseases in obese patients. Therefore, it is our objective to explore experimental studies that approach the relationship between the different types of inflammatory reaction inside the adipose tissue, particularly the macrophage polarization and the development of obesity complications. Further, we intend to speculate how to translate this knowledge, obtained from experimental studies, to treatments applicable to the human diseases. PubMed database was sought using the terms “obesity”, “macrophage” and “polarization”. After applying the filters “Language - English” and “Species - Animals”, we arrived to 90 references. Sixty-two were excluded for being reviews or not related to the main subject. Results in experimental models of obesity pointed a relevant correlation between the macrophage polarization to a type 1 response (M1) inside white adipose tissue and the development of insulin resistance, diabetes and other complications of obesity. Several articles report strategies to shift to a type 2 phenotype (M2), using drugs or lifestyle changes. How these findings could be translated to new human treatments is still an open question that only well designed researches could answer.

scholarly journals Deiodinase Activities in Thyroids and Tissues of Iodine-Deficient Female Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 529-536 ◽  
Author(s):  
Rosalia Lavado-Autric ◽  
Rosa Maria Calvo ◽  
Raquel Martinez de Mena ◽  
Gabriella Morreale de Escobar ◽  
Maria-Jesus Obregon
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Cerebral Cortex ◽  
Brown Adipose Tissue ◽  
Female Rats ◽  
Iodothyronine Deiodinase ◽  
Brown Adipose ◽  
Type 3

Severe iodine deficiency is characterized by goiter, preferential synthesis, and secretion of T3 in thyroids, hypothyroxinemia in plasma and tissues, normal or low plasma T3, and slightly increased plasma TSH. We studied changes in deiodinase activities and mRNA in several tissues of rats maintained on low-iodine diets (LIDs) or LIDs supplemented with iodine (LID+I). T4 and T3 concentrations decreased in plasma, tissues, and thyroids of LID rats, and T4 decreased more than T3 (50%). The highest type 1 iodothyronine deiodinase (D1) activities were found in the thyroid, kidney, and the liver; pituitary, lung, and ovary had lower D1 activities; but the lowest levels were found in the heart and skeletal muscle. D1 activity decreased in all tissues of LID rats (10–40% of LID+I rats), except for ovary and thyroids, which D1 activity increased 2.5-fold. Maximal type 2 iodothyronine deiodinase (D2) activities were found in thyroid, brown adipose tissue, and pituitary, increasing 6.5-fold in thyroids of LID rats and about 20-fold in the whole gland. D2 always increased in response to LID, and maximal increases were found in the cerebral cortex (19-fold), thyroid, brown adipose tissue, and pituitary (6-fold). Lower D2 activities were found in the ovary, heart, and adrenal gland, which increased in LID. Type 3 iodothyronine deiodinase activity was undetectable. Thyroidal Dio1 and Dio2 mRNA increased in the LID rats, and Dio1 decreased in the lung, with no changes in mRNA expression in other tissues. Our data indicate that LID induces changes in deiodinase activities, especially in the thyroid, to counteract the low T4 synthesis and secretion, contributing to maintain the local T3 concentrations in the tissues with D2 activity.

scholarly journals Effects of Peroxisome Proliferator-Activated Receptor-α and -γ Agonists on 11β-Hydroxysteroid Dehydrogenase Type 1 in Subcutaneous Adipose Tissue in Men

2007 ◽  
Vol 92 (5) ◽  
pp. 1848-1856 ◽  
Author(s):  
Deborah J. Wake ◽  
Roland H. Stimson ◽  
Garry D. Tan ◽  
Natalie Z. M. Homer ◽  
Ruth Andrew ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Plasma Cortisol ◽  
Hydroxysteroid Dehydrogenase ◽  
Peroxisome Proliferator ◽  
Cortisol Secretion ◽  
Peroxisome Proliferator Activated Receptor ◽  
Healthy Men ◽  
Pparγ Agonists

Abstract Context: In animals, peroxisome proliferator-activated receptor-α (PPARα) and PPARγ agonists down-regulate 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) mRNA and activity in liver and adipose tissue, respectively, and PPARγ agonists reduce ACTH secretion from corticotrope cells. Objective: Our objective was to test whether PPAR agonists alter cortisol secretion and peripheral regeneration by 11β-HSD1 in humans and whether reduced cortisol action contributes to metabolic effects of PPARγ agonists. Design and Setting: Three randomized placebo-controlled crossover studies were conducted at a clinical research facility. Patients and Participants: Healthy men and patients with type 2 diabetes participated. Interventions, Outcome Measures, and Results: In nine healthy men, 7 d of PPARα agonist (fenofibrate) or PPARγ agonist (rosiglitazone) had no effect on cortisol secretion, hepatic cortisol generation after oral cortisone administration, or tracer kinetics during 9,11,12,12-[2H]4-cortisol infusion, although rosiglitazone marginally reduced cortisol generation in sc adipose tissue measured by in vivo microdialysis. In 12 healthy men, 4–5 wk of rosiglitazone increased insulin sensitivity during insulin infusion but did not change 11β-HSD1 mRNA or activity in sc adipose tissue, and insulin sensitization was unaffected by glucocorticoid blockade with a combination of metyrapone and RU38486. In 12 men with type 2 diabetes 12 wk of rosiglitazone reduced arteriovenous cortisone extraction across abdominal sc adipose tissue and reduced 11β-HSD1 mRNA in sc adipose tissue but increased plasma cortisol concentrations. Conclusions: Neither PPARα nor PPARγ agonists down-regulate 11β-HSD1 or cortisol secretion acutely in humans. The early insulin-sensitizing effect of rosiglitazone is not dependent on reducing intracellular glucocorticoid concentrations. Reduced adipose 11β-HSD1 expression and increased plasma cortisol during longer therapy with rosiglitazone probably reflect indirect effects, e.g. mediated by changes in body fat.

scholarly journals MGL1 promotes adipose tissue inflammation and insulin resistance by regulating 7/4hi monocytes in obesity

2009 ◽  
Vol 206 (13) ◽  
pp. 3143-3156 ◽  
Author(s):  
Daniel J. Westcott ◽  
Jennifer B. DelProposto ◽  
Lynn M. Geletka ◽  
Tianyi Wang ◽  
Kanakadurga Singer ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Critical Role ◽  
Alternatively Activated Macrophages ◽  
Inflammatory Monocytes ◽  
Diet Induced Obesity ◽  
Adipose Tissue Macrophages ◽  
Visceral Adipose

Adipose tissue macrophages (ATMs) play a critical role in obesity-induced inflammation and insulin resistance. Distinct subtypes of ATMs have been identified that differentially express macrophage galactose-type C-type lectin 1 (MGL1/CD301), a marker of alternatively activated macrophages. To evaluate if MGL1 is required for the anti-inflammatory function of resident (type 2) MGL1+ ATMs, we examined the effects of diet-induced obesity (DIO) on inflammation and metabolism in Mgl1−/− mice. We found that Mgl1 is not required for the trafficking of type 2 ATMs to adipose tissue. Surprisingly, obese Mgl1−/− mice were protected from glucose intolerance, insulin resistance, and steatosis despite having more visceral fat. This protection was caused by a significant decrease in inflammatory (type 1) CD11c+ ATMs in the visceral adipose tissue of Mgl1−/− mice. MGL1 was expressed specifically in 7/4hi inflammatory monocytes in the blood and obese Mgl1−/− mice had lower levels of 7/4hi monocytes. Mgl1−/− monocytes had decreased half-life after adoptive transfer and demonstrated decreased adhesion to adipocytes indicating a role for MGL1 in the regulation of monocyte function. This study identifies MGL1 as a novel regulator of inflammatory monocyte trafficking to adipose tissue in response to DIO.

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