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Roles of Daily Diet and Beta-Adrenergic System in the Treatment of Obesity and Diabetes
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Ebru Arioglu Inan, Belma Turan
Curcumin is an active compound of turmeric and its antiobesity effect has been demonstrated in experimental studies (Alappat and Awad 2010; Jimenez-Osorio, Monroy et al. 2016). Its role in obesity has been suggested to be related to its effects on mitochondrial biogenesis. In 3T3-L1 and primary white adipocytes, curcumin caused AMPK activation and peroxisome proliferator activated receptor ɣ coactivator 1α (PGC-1α) upregulation. Furthermore, in adipocytes curcumin increased protein expression of carnitin palmitoyltransferase-1 (CPT-1), hormone sensitive lipase (HSL) and phosphorylation of acetyl-coenzyme A carboxylase (ACC), which further led to attenuated lipid accumulation (Lone, Choi et al. 2016). Animal studies confirmed the beneficial effect of curcumin in obesity as browning of the white adipose tissue was stimulated in curcumin fed C57B/6 mice (Wang, Wang et al. 2015). Uncoupling protein 1 (UCP-1) was also upregulated in these mice. These findings suggest that the antiobesity effect of curcumin may be related to mitochondrial biogenesis in white adipose tissue (Lai, Wu et al. 2015).
Role of Herbs and Spices in Cardiovascular Health
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Haroon Khan, Ada Popolo, Marya, Luca Rastrelli
For thousands of years, algae have been part of the human diet. In addition to their nutritional value, algae are increasingly marketed as “functional foods” or “nutraceuticals”; these terms describe foods that contain bioactive compounds, or phytochemical products that, beyond the basic food role, may represent a health benefit. Macro- and microalgal biomass are an interesting natural source of a great variety of biologically active compounds, such as carotenoids, phycobilins, fatty acids, vitamins, polysaccharides and sterols. Carotenoids consumption is leading to a potential reduction of cardiovascular risk. Carotenoids are associated with blood pressure, reduction of pro-inflammatory cytokines and improvement of insulin sensitivity in muscle, liver and adipose tissues. Fucoxanthin is a carotenoid present in edible brown seaweed (Figure 8.4), and its beneficial effects on cardiovascular diseases were recently reviewed (Gammone et al., 2015). Animal studies have shown that long-term intake of fucoxanthin causes weight loss. For example, in a study conducted by Maeda et al. (2005), it has been shown that fucoxanthin or dried powder of seaweed (Undaria pinnatifida) significantly reduced the white adipose tissue in in Male Wistar rats and female KK-Ay mice after four weeks of treatment. The mechanisms may be related to an upregulation of the mitochondrial uncoupling proteins (UCP) that separate oxidative phosphorylation from ATP synthesis with energy dissipated as heat (Maeda et al., 2005) (Table 8.4).
Noninsulin-Dependent Animal Models of Diabetes Mellitus
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Christopher H. S. McIntosh, Raymond A. Pederson
Several uncoupling proteins have now been identified. The original protein cloned (UCP1) was identified as a membrane proton transporter found in mitochondria, expressed specifically in brown adipose tissue. Activation of the protein results in dissipation of the proton gradient and heat production. DNA polymorphisms in human UCP1 were found to correlate with age-associated increases in body fat.406 Mutations in the protein could lead to reduced energy expenditure and, thus, weight gain. UCP1 knockout mice were shown to consume less oxygen in response to a β3-adrenergic receptor agonist and were more sensitive to cold.407 However, neither obesity nor hyperphagia was observed. Since animals in which BAT had been completely ablated developed marked obesity with increasing age, hyperglycemia, marked hyperinsulinemia, and glucose intolerance,408 the mild pathology of the UCP1 knockout was probably due to compensation by UCP2,409,410 therefore, double knockouts are needed to determine the effect of overall UCP ablation. It is of interest that UCP2 is also found in pancreatic islet β-cells, where it is likely to play a role in insulin secretion, and overexpression of leptin resulted in tenfold increases in UCP2 gene expression.411 This suggests that altered UCP2 expression, resulting from loss of leptin responsiveness, could contribute to the development of obesity/NIDDM.
Current and emerging gluconeogenesis inhibitors for the treatment of Type 2 diabetes
Published in Expert Opinion on Pharmacotherapy, 2021
The many transcription factors involved in gluconeogenesis identified by the use of gene knockout and gene knockdown in mouse models has opened a host of potential targets for drug development. However, transcription factors are not limited in their actions to gluconeogenesis alone. These molecules function in many different processes including tumor development in some cases. Therefore, assurance of the unique action and the safety of potential therapeutic agents is a significant challenge. It is ironic that metformin, the primary drug treatment for Type 2 diabetes, is a very small simple molecule with a large margin of safety [153]. Metformin targets the mitochondrion, and perhaps the greatest opportunities to influence the combined pathways of gluconeogenesis and lipolysis exist in molecules that have mitochondrial effects. The mitochondrion has its own mechanisms including possessing DNA separate from the nucleus. Thus modifications at the mitochondrial pathways may have less detrimental effects than those affecting the cell nucleus. The uncoupling proteins, in particular, have great popular interest due to the thought that they may permit metabolic caloric dissipation rather than adipose accumulation.
Oxidative damage mediated iNOS and UCP-2 upregulation in rat brain after sub-acute cyanide exposure: dose and time-dependent effects
Published in Drug and Chemical Toxicology, 2019
Rahul Bhattacharya, Poonam Singh, Jebin Jacob John, Niranjan L. Gujar
Uncoupling proteins (UCPs) are family of inner mitochondrial membrane proteins that regulate mitochondrial respiration, energy production and ROS generation by catalyzing an inner membrane protein leak. UCP-2 is the most ubiquitously present inner mitochondrial membrane proton carrier that modulates mitochondrial membrane potential (MMP; Δψm) and uncouples oxidative phosphorylation, leading to impaired ATP synthesis (Erlanson-Albertsson 2003). Upregulation of UCP-2 by cyanide has been associated with mitochondrial dysfunction, activation of peroxisome proliferator-activated receptor-alpha (PPARα), and oxidative stress leading to cell death (Li et al. 2005, Prabhakaran et al. 2005, Zhang et al. 2007). However, all these studies have been performed in vitro employing different cell lines. The present study was designed to assess the dose- and time-dependent effects of cyanide on various biochemical indices, including the oxidative stress markers, UCP-2 and iNOS expression, and DNA damage in rats after sub-acute exposure. The study intends to highlight the involvement of chemical hypoxia mediated oxidative damage in the upregulation of iNOS and UCP-2 expression after repeated cyanide exposure in rat.
CNR2 rs2229579 and COMT Val158Met variants, but not CNR2 rs2501432, IL-17 rs763780 and UCP2 rs659366, contribute to susceptibility to substance use disorder in the Turkish population
Published in Psychiatry and Clinical Psychopharmacology, 2019
Selin Kurnaz, Ahmet Bulent Yazici, Ayse Feyda Nursal, Pinar Cetinay Aydin, Ayca Ongel Atar, Nazan Aydin, Zeliha Kincir, Sacide Pehlivan
Catechol-O-methyltransferase (COMT) is an enzyme found all over the mammalian central nervous system which breaks down the catecholamine neurotransmitters dopamine, epinephrine, and norepinephrine. A common G-to-A transition in exon 4 of the COMT gene, causing a valine (val)-to-methionine (met) substitution at the amino acid position 108 or 158 (depending on the splice variant), results in a four-fold reduction in enzyme activity in met homozygotes, whereas heterozygotes manifest intermediate activity [3]. The endocannabinoid system plays a role in susceptibility to substance abuse. There are two well-defined cannabinoid receptors (CNRs), CNR1/CB1 and CNR2/CB2, that mediate endocannabinoid signalling [4]. CNR2 has been classically defined as the peripheral cannabinoid receptor because CNR2 is expressed principally in some peripheral and immune cells [5]. Uncoupling protein 2 (UCP2) is a member of an anion-carrier protein family found in the mitochondrial inner membrane. In the central nervous system, mammalian UCP2 mRNA and protein expression occurs at highest levels in regions that could be described as high-risk for stress [6]. The Interleukin 17 (IL-17 or IL-17A) is a fundamental pro-inflammatory cytokine that is primarily released from T cells and is now believed to be the defining cytokine of a recently discovered new subset of T-helper cells, Th17 [7]. New studies have reported that cells of the central nervous system also express IL-17.