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The introduction of newborn screening and the development of new therapies have led to an expanding population of patients with inherited metabolic disorders, and these patients are now entering adulthood. Dietary therapy is the m...
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The introduction of newborn screening and the development of new therapies have led to an expanding population of patients with inherited metabolic disorders, and these patients are now entering adulthood. Dietary therapy is the mainstay of treatment for many of these disorders, and thus, trained metabolic dietitians are critical members of the multidisciplinary team required for management of such patients. The main goals of dietary therapy in inborn errors of metabolism are the maintenance of normal growth and development while limiting offending metabolites and providing deficient products. Typically, the offending metabolite is either significantly reduced or removed completely from the diet and then reintroduced in small quantities until blood levels are within the normal range. Such treatment is required in infancy, childhood, and adulthood and requires careful monitoring of micronutrient and macronutrient intake throughout the life span. The goal of this review is to highlight the basic principles of chronic nutrition management of the inborn errors of protein, carbohydrate, and fat metabolism.
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Abstract A prospective randomized phase II trial was conducted to evaluate the time course effects of toremifene (TOR) and letrozole (LET), as adjuvant hormone therapy, on serum lipid profiles and bone metabolism in estrogen recep...
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Abstract A prospective randomized phase II trial was conducted to evaluate the time course effects of toremifene (TOR) and letrozole (LET), as adjuvant hormone therapy, on serum lipid profiles and bone metabolism in estrogen receptor (ER)-positive, postmenopausal breast cancer patients.Fifty-four postmenopausal breast cancer patients [ER positive, HER2 negative, T1–2, node metastases ( n ?=?0–3), M0] who had undergone curative resection were enrolled. They were randomized to receive either TOR 40?mg/day or LET 2.5?mg/day as adjuvant hormone therapy. Serum lipids and bone markers were measured prior to, and again at 6, 12, and 24?months after initiation of treatment. Changes in serum lipids and bone markers were compared. Serum levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were decreased compared with the baseline values at 6 months in 6.5 and 14.0% of patients, respectively, receiving TOR. Lipid levels did not change in patients administered LET. Significant differences were observed in TC and LDL-C between the two groups at 12 and 24?months. In the TOR group, serum bone-specific alkaline phosphatase (BAP) was decreased by 25.0% at 12 months, and serum cross-linked N-telopeptide of type-I collagen (NTx) was decreased by 13.6% at 6?months, and these reductions were maintained for at least 24?months. In contrast, in the LET group, serum BAP did not change and NTx was increased by 16.0% at 6?months and by 18.6% at 24 months, as compared with the baseline.TOR and LET exert different effects on serum lipid profiles and bone metabolism markers. The effects of TOR, as adjuvant hormone therapy, on both lipids and bone metabolism in postmenopausal breast cancer patients are superior to those of LET.
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Metabolic myopathies are disorders affecting utilization of carbohydrates or fat in the skeletal muscle. Adult patients with metabolic myopathies typically present with exercise-induced pain, contractures or stiffness, fatigue, an...
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Metabolic myopathies are disorders affecting utilization of carbohydrates or fat in the skeletal muscle. Adult patients with metabolic myopathies typically present with exercise-induced pain, contractures or stiffness, fatigue, and myoglobinuria. Symptoms are related to energy failure.
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-oxidation needs during tumor proliferation and metastasis. The common induction of metabolic pathways during cancer progression, regardless of cancer histio- or genotype, makes cancer metabolism an attractive target for therapeut...
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-oxidation needs during tumor proliferation and metastasis. The common induction of metabolic pathways during cancer progression, regardless of cancer histio- or genotype, makes cancer metabolism an attractive target for therapeutic exploitation. Recent Advances: Emerging data suggest that these altered pathways may even result in resistance to anticancer therapies. Identifying specific metabolic dependencies that are unique to cancer cells has proved challenging in this field, limiting the therapeutic window for many candidate drug approaches. Critical Issues: Cancer cells display significant metabolic flexibility in nutrient-limited environments, hampering the longevity of suppressing cancer metabolism through any singular approach. Combinatorial "synthetic lethal" approaches may have a better chance for success and promising strategies are reviewed here. The dynamism of the immune system adds a level of complexity, as various immune populations in the tumor microenvironment often share metabolic pathways with cancer, with successive alterations during immune activation and quiescence. Decoding the reprogramming of metabolic pathways within cancer cells and stem cells, as well as examining metabolic symbiosis between components of the tumor microenvironment, would be essential to further meaningful drug development within the tumor's metabolic ecosystem. Future Directions: In this article, we examine evidence for the therapeutic potential of targeting metabolic alterations in cancer, and we discuss the drawbacks and successes that have stimulated this field.
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The network for cardiac fuel metabolism contains intricate sets of interacting pathways that result in both ATP-producing and non-ATP-producing end points for each class of energy substrates. The most salient feature of the networ...
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The network for cardiac fuel metabolism contains intricate sets of interacting pathways that result in both ATP-producing and non-ATP-producing end points for each class of energy substrates. The most salient feature of the network is the metabolic flexibility demonstrated in response to various stimuli, including developmental changes and nutritional status. The heart is also capable of remodeling the metabolic pathways in chronic pathophysiological conditions, which results in modulations of myocardial energetics and contractile function. In a quest to understand the complexity of the cardiac metabolic network, pharmacological and genetic tools have been engaged to manipulate cardiac metabolism in a variety of research models. In concert, a host of therapeutic interventions have been tested clinically to target substrate preference, insulin sensitivity, and mitochondrial function. In addition, the contribution of cellular metabolism to growth, survival, and other signaling pathways through the production of metabolic intermediates has been increasingly noted. In this review, we provide an overview of the cardiac metabolic network and highlight alterations observed in cardiac pathologies as well as strategies used as metabolic therapies in heart failure. Lastly, the ability of metabolic derivatives to intersect growth and survival are also discussed.
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Metabolic reprogramming contributes to tumor development and introduces metabolic liabilities that can be exploited to treat cancer. Chemotherapies targeting metabolism have been effective cancer treatments for decades, and the su...
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Metabolic reprogramming contributes to tumor development and introduces metabolic liabilities that can be exploited to treat cancer. Chemotherapies targeting metabolism have been effective cancer treatments for decades, and the success of these therapies demonstrates that a therapeutic window exists to target malignant metabolism. New insights into the differential metabolic dependencies of tumors have provided novel therapeutic strategies to exploit altered metabolism, some of which are being evaluated in preclinical models or clinical trials. Here, we review our current understanding of cancer metabolism and discuss how this might guide treatments targeting the metabolic requirements of tumor cells.
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? 2021 Elsevier B.V.Fatty liver disease (FLD) is one of the largest burdens to human health worldwide and is associated with gut microbiome and metabolite stability. Engineered liver tissues have shown promise in restoring liver f...
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? 2021 Elsevier B.V.Fatty liver disease (FLD) is one of the largest burdens to human health worldwide and is associated with gut microbiome and metabolite stability. Engineered liver tissues have shown promise in restoring liver functions in non-alcoholic FLD (NAFLD), hepatitis and cirrhosis. Fatty liver, largely noted in obesity and hepatic cancer, is highly fatal and has led to a global increase in death rates. It is associated with complex metabolic reprogramming too. A standard approach to therapy in the newly diagnosed setting includes surgery or identification of biomarkers/ metabolites for therapeutic purposes, which ultimately focus on improvement of liver health in patients. As such there are no standard procedures for patient care, but depending on the severity, systemic therapy with either genomic, proteomic or metabolomic profiling form potential options. Better comparisons and study of underlying mechanisms in gut microbiome-based metabolic functions in obesity are urgently required. Today, an emerging field, focusing on metabolomic approaches and metabolic phenotyping, involved in high-throughput identification of metabolome in obesity and gut disorders, is involved in biomarker and metabolite identification. There are supporting technologies and approaches in NAFLD that throw light on the metabolites and gut microbiome, and also on the understanding of the risk factors of obesity along with liver cancer metabolic reaction networks. We discuss the current state of NAFLD metabolites, gut micro-environmental changes, and the further challenges in digital metabolomics profiling. Innovative clinical trial designs, with biomarker-enrichment strategies that are required to improve the outcome of NAFLD in patients are also discussed.
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The prevalence of metabolic Syndrome (MetS) in men with benign prostatic hyperplasia (BPH) asreported by Asian Studies was 26.7% to 55.4%, Men with MetS have higher prostate volume and higherprostate growth rate. Insulin resistanc...
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The prevalence of metabolic Syndrome (MetS) in men with benign prostatic hyperplasia (BPH) asreported by Asian Studies was 26.7% to 55.4%, Men with MetS have higher prostate volume and higherprostate growth rate. Insulin resistance, increased visceral adiposity, low androgen high estrogenlevels, low grade inflammatory state, dyslipidemia are all contributory factors. The treatment optionsinclude lifestyle modification, alpha 1 adrenoreceptor blocker, 5 alpha reductase inhibitors, PDE5inhibitors. Combination of 5 α reductase inhibitors and α-blockers provides relief to LUTS and preventsprogression of BPH.
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Purpose Somatostatin receptor-targeted radiopeptide therapy is commonly performed using single radioisotopes. We evaluated the benefits and harms of combining radioisotopes in radiopeptide therapy in pat...
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Purpose Somatostatin receptor-targeted radiopeptide therapy is commonly performed using single radioisotopes. We evaluated the benefits and harms of combining radioisotopes in radiopeptide therapy in patients with neuroendocrine tumor.
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