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Mitigation of Obesity: A Phytotherapeutic Approach
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
A.B. Sharangi, Suddhasuchi Das
Adipocytes release fatty acid, which are used as fuel by organs in times of limited glucose. These fatty acids are the outcomes from triacylglycerol breakdown, which contain more energy per unit mass compared to carbohydrates. Lipid homeostasis and energy balance is centrally regulated by adipocytes. According to changing energy demands they release free fatty acids from stored triglycerides. The hyperplasia and hypertrophy of adipocytes both are involved with adipocyte tissue growth, which led to the development of natural products which helps in anti-obesity therapy that exclusively target adipogenesis inhibition. Some research has also proposed that through blockade of several transcription factors like C/EBP_ (CCAAT/enhancer-binding protein beta) and PPAR (peroxisome proliferator-activated receptor-gamma) adipocyte differentiation could be inhibited (Kang et al., 2013).
An Asian woman with blurred vision
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
Rosiglitazone and pioglitazone also target insulin resistance but through a different mechanism. These drugs are peroxisome proliferator-activated receptor-gamma (PPAR) agonists. PPAR receptors are found in tissues important for insulin action such as adipose tissue, skeletal muscle, and liver.
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Published in Henry J. Woodford, Essential Geriatrics, 2022
Thiazolidinediones (e.g. pioglitazone) stimulate peroxisome proliferator-activated receptor-gamma, which causes increased transcription of insulin-sensitive genes and are sometimes termed ‘insulin sensitisers', i.e. reduced insulin resistance. They may provoke oedema and are not recommended for people with heart failure. They have been associated with an increased risk of fractures.107 They may also increase the risk of bladder cancer. A trial comparing pioglitazone to placebo (n = 5,238; mean age 62) found that it reduced HbA1C (7.0% v 7.6%) but this did not lead to a significant benefit in the primary outcome of combined mortality and vascular events (HR 0.90; 95% CI 0.08–1.02).108 It did, however, lead to an increased incidence of heart failure (11% v 8%) and weight gain (average 3.6 kg v –0.4 kg). For all of these reasons, this class of medications is rarely indicated in older adults.
PPARG, GNG12, and CD19 are potential independent predictors of central nerve recurrence in childhood acute lymphoblastic leukemia
Published in Hematology, 2023
Shan Zhang, Yansong Tu, Hurong Lai, Huijun Chen, Huaijun Tu, Jian Li
PPARG gene is a member of the nuclear receptor family, which encodes peroxisome proliferative activated receptor gamma (PPARγ), PPARγ was first identified in adipocytes, as a transcription factor, the PPARγ receptor binds to its ligand, inhibits tumor proliferation, metastasis, and angiogenesis, and promotes apoptosis and immune regulation by activating signaling pathways of different tumor cells and tumor stem cells [18]. For example, PPARγ can induce apoptosis by inhibiting the PI3K/Akt signaling pathway, PPARγ ligand can induce the apoptosis of leukemia cells, and can be potentially used to treat hematologic malignancies, especially leukemia [19]. In our study, we found a low expression of PPARG in childhood ALL with CNS relapse. Moreover, KEGG analysis showed the activation of the PI3K/Akt signaling pathway, which suggests that PPARG might regulate CNS relapse in ALL children through the PI3K/Akt signaling pathway. Boyd et al. [20] found that the injection of PPARS antibody agonist could induce adipogenesis in bone marrow tissue in mice, thereby saving healthy hematopoietic cell formation during the inhibition of leukemia cell growth. The most common way leukemia cells invade the central nervous system is from the bone marrow of the skull to the subarachnoid space via dural bridging vein [21]. When the expression of the PPARG gene is low, this induction function of PPARs is inhibited, which might in turn lead to the CNS relapse of ALL in children.
Serum claudin-5, claudin-11, occludin, vinculin, paxillin, and beta-catenin levels in preschool children with autism spectrum disorder
Published in Nordic Journal of Psychiatry, 2023
Ayhan Bilgiç, Hurşit Ferahkaya, Hülya Karagöz, İbrahim Kılınç, Vesile Meltem Energin
We found higher serum β- catenin levels in children with ASD than in the control group. To our knowledge, this is the first study to investigate the circulating β- catenin levels in ASD subjects. However, a variety of studies provided data regarding the potential role of β- catenin in ASD. Several ASD-linked gene mutations are predicted to change β-catenin functions [12,29,46,47]. In a recent study, Alexander et al. demonstrated that excessive β –catenin expression leads to decreased social interest and increased repetitive behaviors in mice [33]. This study also found decreased parvalbumin and altered levels of other genes that were identified as potential risk factors for ASD in humans. Further support for a potential role of Wnt/β -catenin signaling in ASD comes from pharmacological studies. The peroxisome proliferator-activated receptor gamma (PPAR γ) and canonical WNT/β-catenin pathway act in an opposed manner and preliminary data suggest that PPAR γ agonists may have a positive effect in the treatment for ASD children [48]. Considering the role of Wnt/β-catenin pathway in endothelial barrier functions, an alteration in this pathway can lead to an impairment in blood-brain and intestinal barriers functionality in ASD. The link between Wnt/β-catenin pathway and ASD must be evaluated through additional studies.
PPAR Receptors Expressed from Vectors Containing CMV Promoter Can Enhance Self-Transcription in the Presence of Fatty Acids from CLA-Enriched Egg Yolks—A Novel Method for Studies of PPAR Ligands
Published in Nutrition and Cancer, 2020
Aneta A. Koronowicz, Adam Master, Paula Banks, Ewelina Piasna-Słupecka, Dominik Domagała, Mariola Drozdowska, Teresa Leszczyńska
Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors belonging to the steroid hormone nuclear receptor superfamily. Initially, PPARs were first described as nuclear receptors for synthetic substances that induced the proliferation of peroxisomes. Shortly after, it was realized that many natural and synthetic substances act selectively through these receptors (1) and that in fact, PPARs encompass a group of three main protein isoforms PPARα, PPARβ/δ, and PPARγ (2) encoded by PPARA, PPARD, and PPARG genes. All these transcription factors are composed of four functional domains including an N-terminal A/B domain (AF1, containing activation function 1), a DNA-binding domain (DBD) containing two zinc fingers, a hinge domain, and a C-terminal ligand-binding domain (LBD, containing activation function 2, AF2). DBD of all PPAR isoforms can bind to the same peroxisome proliferator-activated receptor response element (PPRE) that are specific DNA sequences of the typical consensus core recognition motif AGGTCANAGGTCA (DR1), however, some non-canonical PPREs have been described (3). Apart from binding of ligands, PPAR LBD allows for heterodimerization with other nuclear receptors including retinoid X receptor (RXR) and this complex subsequently recruits corepressors or coactivators, to regulate the expression of target genes responding to receptors liganded by various small lipophilic ligands (4).