scholarly journals Antiretroviral-Related Adipocyte Dysfunction and Lipodystrophy in HIV-Infected Patients: Alteration of the PPARγ-Dependent Pathways

PPAR Research ◽  
2009 ◽  
Vol 2009 ◽  
pp. 1-8 ◽  
Author(s):  
Martine Caron ◽  
Corinne Vigouroux ◽  
Jean-Philippe Bastard ◽  
Jacqueline Capeau
Keyword(s):  
Adipose Tissue ◽  
Cell Function ◽  
Nuclear Translocation ◽  
Fat Tissue ◽  
Related Function ◽  
Adipose Cell ◽  
Cell Dysfunction ◽  
Mrna And Protein Expression ◽  
A Cell

Lipodystrophy and metabolic alterations are major complications of antiretroviral therapy in HIV-infected patients. In vitro studies using cultured murine and human adipocytes revealed that some protease inhibitors (PIs) and nucleoside reverse transcriptase inhibitors (NRTIs) were implicated to a different extent in adipose cell dysfunction and that a chronic incubation with some PIs decreased mRNA and protein expression of PPARγ. Defective lamin A maturation linked to PI inhibitory activity could impede the nuclear translocation of SREBP1c, therefore, reducing PPARγexpression. Adipose cell function was partially restored by the PPARγagonists, thiazolidinediones. Adverse effects of PIs and NRTIs have also been reported in macrophages, a cell type that coexists with, and modulates, adipocyte function in fat tissue. In HIV-infected patients under ART, a decreased expression of PPARγand of PPARγ-related genes was observed in adipose tissue, these anomalies being more severe in patients with ART-induced lipoatrophy. Altered PPARγexpression was reversed in patients stopping PIs. Treatment of patients with agonists of PPARγcould improve, at least partially, the subcutaneous lipoatrophy. These data indicate that decreased PPARγexpression and PPARγ-related function, resulting from ART-induced adipose tissue toxicity, play a central role in HIV-related lipoatrophy and metabolic consequences.

scholarly journals Cellular effects of glycine and trehalose air-polishing powders on human gingival fibroblasts in vitro

2021 ◽  
Author(s):  
Jens Weusmann ◽  
James Deschner ◽  
Jean-Claude Imber ◽  
Anna Damanaki ◽  
Natalia D. P. Leguizamón ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Function ◽  
Nuclear Translocation ◽  
In Vitro Study ◽  
Human Gingival Fibroblasts ◽  
Mrna Levels ◽  
Gingival Fibroblasts ◽  
Air Polishing ◽  
Wide Range

Abstract Objectives Air-polishing has been used in the treatment of periodontitis and gingivitis for years. The introduction of low-abrasive powders has enabled the use of air-polishing devices for subgingival therapy. Within the last decade, a wide range of different low-abrasive powders for subgingival use has been established. In this study, the effects of a glycine powder and a trehalose powder on human gingival fibroblasts (HGF) were investigated. Methods HGF were derived from three systemically and periodontally healthy donors. After 24 h and 48 h of incubation time, mRNA levels, and after 48 h, protein levels of TNFα, IL-8, CCL2, and VEGF were determined. In addition, NF-κB p65 nuclear translocation and in vitro wound healing were assessed. Statistical analysis was performed by ANOVA and post hoc Dunnett’s and Tukey’s tests (p < 0.05). Results Glycine powder significantly increased the expression of proinflammatory genes and showed exploitation of the NF-κB pathway, albeit trehalose powder hardly interfered with cell function and did not trigger the NF-κB pathway. In contrast to trehalose, glycine showed a significant inhibitory effect on the in vitro wound healing rate. Conclusion Subgingivally applicable powders for air-polishing devices can regulate cell viability and proliferation as well as cytokine expression. Our in vitro study suggests that the above powders may influence HGF via direct cell effects. Trehalose appears to be relatively inert compared to glycine powder.

scholarly journals Cellular adaptations in fat tissue of exercise-trained miniature swine: role of excess energy intake

2000 ◽  
Vol 88 (3) ◽  
pp. 881-887 ◽  
Author(s):  
Gale B. Carey
Keyword(s):  
Adipose Tissue ◽  
Energy Intake ◽  
Excess Energy ◽  
Fat Tissue ◽  
Cellular Mechanisms ◽  
Miniature Swine ◽  
Extracellular Adenosine

This study examined the influence of energy expenditure and energy intake on cellular mechanisms regulating adipose tissue metabolism. 1 Twenty-four swine were assigned to restricted-fed sedentary, restricted-fed exercise-trained, full-fed sedentary, or full-fed exercise-trained groups. After 3 mo of treatment, adipocytes were isolated and adipocyte size, adenosine A1 receptor characteristics, and lipolytic sensitivity were measured. Swine were infused with epinephrine during which adipose tissue extracellular adenosine, plasma fatty acids, and plasma glycerol were measured. Results revealed that adipocytes isolated from restricted-fed exercised swine had a smaller diameter, a lower number of A1 receptors, and a greater sensitivity to lipolytic stimulation, compared with adipocytes from full-fed exercised swine. Extracellular adenosine levels were transiently increased on infusion of epinephrine in adipose tissue of restricted-fed exercised but not full-fed exercised swine. These results suggest a role for adenosine in explaining the discrepancy between in vitro and in vivo lipolysis findings and underscore the notion that excess energy intake dampens the lipolytic sensitivity of adipocytes to β-agonists and adenosine, even if accompanied by exercise training.

RELATIONSHIPS BETWEEN CALCIUM TRANSPORT AND THE LIPOLYTIC EFFECT OF SHEEP β-LIPOTROPIC HORMONE β-LPH) IN ADIPOSE TISSUE

1972 ◽  
Vol 69 (3) ◽  
pp. 507-516 ◽  
Author(s):  
M. Lis ◽  
C. Gilardeau ◽  
M. Chrétien
Keyword(s):  
Adipose Tissue ◽  
Intravenous Injection ◽  
Calcium Transport ◽  
Lipolytic Activity ◽  
Fat Cells ◽  
Tetraacetic Acid ◽  
Isolated Fat Cells ◽  
Fat Tissue ◽  
Adipose Cell ◽  
Epididymal Fat

ABSTRACT Intravenous injection of β-lipotropic hormone β-LPH) into rabbits caused a marked increase of Ca++ concentration in perirenal or epididymal fat tissue. β-LPH also increased the amount of Ca++ taken up during incubation of isolated fat cells. Incubation of fragments of rabbit fat tissue in presence of 45Ca and 3H mannitol indicated that Ca++ accumulated intra-cellularly after administration of β-LPH. In incubation media containing no Ca++, or containing Ca++ and the Ca++ sequestering agent EGTA (ethylenebis [oxyethylene nitrilo]-tetraacetic acid), β-LPH did not induce lipolysis. Addition of excess Ca++ to the EGTA containing medium restored lipolysis, whereas addition of EGTA to incubation mixtures containing Ca++ in which lipolysis in the presence of β-LPH was already proceeding stopped the lipolytic reaction. These results indicated that Ca++ is essential for lipolytic activity of β-LPH as it is for the lipolytic activity of ACTH and other structurally related peptides. Marked shift of Ca++ towards the adipose cell was correlated with β-LPH induced lipolysis.

scholarly journals Adipose Tissue-Derived Microvascular Fragments From Male and Female Fat Donors Exhibit a Comparable Vascularization Capacity

2021 ◽  
Vol 9 ◽  
Author(s):  
Thomas Später ◽  
Julia E. Marschall ◽  
Lea K. Brücker ◽  
Ruth M. Nickels ◽  
Wolfgang Metzger ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Experimental Studies ◽  
Length Distribution ◽  
Fat Tissue ◽  
Male And Female ◽  
Thickness Skin ◽  
Future Clinical Practice ◽  
Male Donor ◽  
Female Donor

Adipose tissue-derived microvascular fragments (MVF) represent effective vascularization units for tissue engineering. Most experimental studies exclusively use epididymal fat tissue of male donor mice as a source for MVF isolation. However, in future clinical practice, MVF-based approaches may be applied in both male and female patients. Therefore, we herein compared the vascularization capacity of MVF isolated from the epididymal and peri-ovarian fat tissue of male and female donor mice. Freshly isolated MVF from male and female donors did not differ in their number, length distribution, viability and cellular composition. After their assembly into spheroids, they also exhibited a comparable in vitro sprouting activity. Moreover, they could be seeded onto collagen-glycosaminoglycan matrices, which were implanted into full-thickness skin defects within mouse dorsal skinfold chambers. Repetitive intravital fluorescence microscopy as well as histological and immunohistochemical analyses revealed a comparable vascularization and incorporation of implants seeded with MVF of male and female origin. Taken together, these findings demonstrate that the vascularization capacity of MVF is not gender-specific.

scholarly journals OPTICAL COHERENCE TOMOGRAPHY OF ADIPOSE TISSUE AT PHOTODYNAMIC/PHOTOTHERMAL TREATMENT IN VITRO

2013 ◽  
Vol 06 (02) ◽  
pp. 1350010 ◽  
Author(s):  
IRINA YU. YANINA ◽  
NATALIA A. TRUNINA ◽  
VALERY V. TUCHIN
Keyword(s):  
Adipose Tissue ◽  
Brilliant Green ◽  
Light Exposure ◽  
Fat Tissue ◽  
Fat Cell ◽  
Refractive Index Distribution ◽  
Tissue Slices ◽  
Photothermal Treatment ◽  
Index Distribution

Temporal changes in structure and refractive-index distribution of adipose tissue at photodynamic/photothermal treatment were studied with OCT in vitro. Ethanol–water solutions of indocyanine green (ICG) and brilliant green (BG) were used for fat tissue staining. CW laser diode (808 nm) and LED light source (442 and 597 nm) were used for irradiation of stained tissue slices. The data received supporting the hypothesis that photodynamic/photothermal treatment, induces fat cell lipolysis during a certain period of time after light exposure.

Adipose tissue can be generated in vitro by using adipocytes from human fat tissue mesenchymal stem cells seeded and cultured on fibrin gel sheet

2012 ◽  
Vol 14 (1) ◽  
pp. 97-106 ◽  
Author(s):  
Cong Toai Tran ◽  
Duy Thao Huynh ◽  
Ciro Gargiulo ◽  
Le Bao Ha Tran ◽  
Minh Hang Huynh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Adipose Tissue ◽  
Fat Tissue ◽  
Fibrin Gel

scholarly journals Induction of core circadian clock transcription factor Bmal1 enhances β cell function and protects against obesity-induced glucose intolerance

2020 ◽  
Author(s):  
Ada Admin ◽  
Kuntol Rakshit ◽  
Aleksey V. Matveyenko
Keyword(s):  
Transcription Factor ◽  
Insulin Secretion ◽  
Circadian Clock ◽  
Glucose Intolerance ◽  
Target Genes ◽  
Cell Function ◽  
Dependent Manner ◽  
Β Cell ◽  
Cell Dysfunction

Type 2 diabetes mellitus (T2DM) is characterized by β cell dysfunction due to impaired glucose-stimulated insulin secretion (GSIS). Studies show that β cell circadian clocks are important regulators of GSIS and glucose homeostasis. These observations raise the question whether enhancement of the circadian clock in β cells will confer protection against β cell dysfunction under diabetogenic conditions. To test this we employed an approach by first generating mice with β cell-specific inducible overexpression of <i>Bmal1</i> (core circadian transcription factor; <i>β-Bmal1<sup>OV</sup></i>). We subsequently examined the effects of <i>β-Bmal1<sup>OV</sup> </i>on the circadian clock, GSIS, islet transcriptome, and glucose metabolism in context of diet-induced obesity. We additionally tested the effects of circadian clock-enhancing small molecule Nobiletin on GSIS in mouse and human control and T2DM islets. We report that <i>β-Bmal1<sup>OV</sup> </i>mice display<i> </i>enhanced islet circadian clock amplitude, augmented <i>in vivo</i> and <i>in vitro</i> GSIS and are protected against obesity-induced glucose intolerance. These effects were associated with increased expression of purported BMAL1-target genes mediating insulin secretion, processing, and lipid metabolism. Furthermore, exposure of isolated islets to Nobiletin enhanced β cell secretory function in <i>Bmal1</i>-dependent manner. This work suggests therapeutic targeting of the circadian system as a potential strategy to counteract β cell failure under diabetogenic conditions.

scholarly journals Preliminary studies for an immunotherapeutic approach to the treatment of human myeloma using chimeric anti-CD38 antibody

Blood ◽  
1991 ◽  
Vol 77 (5) ◽  
pp. 1071-1079 ◽  
Author(s):  
FK Stevenson ◽  
AJ Bell ◽  
R Cusack ◽  
TJ Hamblin ◽  
CJ Slade ◽  
...  
Keyword(s):  
Plasma Cells ◽  
Cell Function ◽  
Detailed Examination ◽  
Chimeric Antibody ◽  
Effector Cells ◽  
Normal Individuals ◽  
A Cell ◽  
Human Igg1 ◽  
Cd38 Antigen

Multiple myeloma is a disease in which conventional chemotherapy has only limited value, but which may be ideal for treatment with passive antibody against a suitable cell surface antigen on the neoplastic plasma cell. The CD38 antigen is known to be present on the majority of neoplastic plasma cells, and this was confirmed by detailed examination of bone marrow aspirates from three patients. Strong expression of CD38 was confined to cells which, by the criteria of light-scattering profiles and possession of cytoplasmic Ig, were plasma cells. The vast majority of neoplastic plasma cells appeared to be involved. Using a cell line as a model, it was found that the CD38 antigen acts as a target for a chimeric antibody prepared from the antibody OKT10. The chimeric antibody consists of the Fab portion of the mouse monoclonal antibody linked by a stable thioether bond to an Fc molecule derived from human IgG1, thereby forming mouse Fab-human Fc. In contrast to the parent antibody, the chimeric molecule mediates antibody-dependent cellular cytotoxicity (ADCC) very efficiently with human blood mononuclear effector cells, and is effective at low concentration. Also, even though the CD38 antigen is present on natural killer cells, there appears to be little deleterious action of the antibody on effector cell function. The antibody also failed to affect the growth of progenitor cells of the granulocyte/macrophage or erythroid lineages present in normal bone marrows, despite the suspicion that these cells express the antigen. Other advantages of the CD38 molecule are that it is not found in the serum of patients with myeloma, and it does not appear to modulate in vitro. Fourteen patients with florid myeloma and on various chemotherapeutic regimes had an undiminished capacity to mediate ADCC with the chimeric antibody, when compared with normal individuals. The maintenance of ADCC activity, coupled with the known suppression of the antibody response in these patients, augers well for treatment with chimeric antibody.

Lipid metabolism in finishing bulls and steers implanted with oestradiol-17 β-dipropionate

1983 ◽  
Vol 37 (1) ◽  
pp. 81-88 ◽  
Author(s):  
R. L. Prior ◽  
S. B. Smith ◽  
B. D. Schanbacher ◽  
H. J. Mersmann
Keyword(s):  
Adipose Tissue ◽  
Coenzyme A ◽  
Experimental Treatment ◽  
Cell Number ◽  
Aconitate Hydratase ◽  
Acetyl Coenzyme A ◽  
Adipose Cell ◽  
Acetyl Coenzyme ◽  
Acetyl Coenzyme A Carboxylase

ABSTRACTTwenty bull calves were assigned to one of four treatment groups: 1) intact bulls; 2) intact bulls implanted with oestradiol dipropionate; 3) steers, and 4) steers implanted with oestradiol dipropionate. Subcutaneous adipose tissue was obtained by biopsy 5 months after implantation. Experimental treatment did not alter (P > 0·05) mean adipose cell volume, diameter or cell number per g adipose tissue. Soluble protein content of adipose cells from bulls was increased by implantation, but not in steers. In vitro rates of fatty acid synthesis were higher in oestrogen-implanted cattle compared with nonimplanted cattle when expressed per g adipose tissue, but not when expressed per cell. Maximal activities of the lipogenic-related enzymes, acetyl coenzyme A carboxylase, adenosine triphosphate-citrate lyase, aconitate hydratase and NADP-isocitrate dehydrogenase were higher in implanted compared with nonimplanted cattle when the activities were expressed per g tissue and acetyl coenzyme A carboxylase and aconitase were also higher when expressed per adipose cell. Bulls and steers had the same basal and stimulated lipolytic rates and implantation of oestradiol dipropionate had no effect on either basal or stimulated lipolytic rate. In this experiment, the oestrogenic implant appeared to have a stimulatory effect on in vitro estimates of lipogenesis.

scholarly journals Berberine Potentiates Insulin Secretion and Prevents β-cell Dysfunction Through the miR-204/SIRT1 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaoyan Lv ◽  
Yali Zhao ◽  
Xuehan Yang ◽  
Hao Han ◽  
Yue Ge ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Palmitic Acid ◽  
Cell Function ◽  
Therapeutic Effects ◽  
Β Cells ◽  
Β Cell ◽  
Sirt1 Expression ◽  
Min6 Cells ◽  
Cell Dysfunction

Pancreatic β-cell dysfunction is a key link during the progression of type 2 diabetes (T2DM), and SIRT1 participates in the regulation of various physiological activities of islet β-cells. However, as a key link in signal transduction, it is not clear how SIRT1 is regulated. By TargetScan prediction, we found that miR-204, which is enriched in islets, has highly complementary binding sites with SIRT1. Therefore, we speculate that miR-204 may be the upstream regulatory target of SIRT1 in islets and thus participate in the occurrence of β-cell dysfunction. In this study, we explored the association between miR-204 and β-cell dysfunction, the therapeutic effects of berberine (BBR) on β-cell function and the possible mechanisms. We found that miR-204 increased and SIRT1 mRNA and protein levels decreased significantly in islets both in vivo and in vitro. MIN6 cells induced by palmitic acid exhibited increased apoptosis, and the accumulation of insulin and ATP in the supernatant decreased. Importantly, palmitic acid treatment combined with miR-204 silencing showed opposite changes. MiR-204 overexpression in MIN6 cells increased apoptosis and decreased insulin and ATP production and SIRT1 expression. SIRT1 overexpression reversed the damage to β-cells caused by miR-204. The BBR treatment effectively improved insulin synthesis, reduced miR-204 levels, and increased SIRT1 expression in islet tissue in diabetic mice. Overexpression of miR-204 reversed the protective effect of BBR on apoptosis and insulin secretion in MIN6 cells. Our study identifies a novel correlation between miR-204 and β-cell dysfunction in T2DM and shows that administration of BBR leads to remission of β-cell dysfunction by regulating the miR-204/SIRT1 pathway.

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