-
Frontiers in Endocrinology 2023Recent research has emphasized the interaction between the circadian clock and lipid metabolism, particularly in relation to tumors. This review aims to explore how the... (Review)
Review
Recent research has emphasized the interaction between the circadian clock and lipid metabolism, particularly in relation to tumors. This review aims to explore how the circadian clock regulates lipid metabolism and its impact on carcinogenesis. Specifically, targeting key enzymes involved in fatty acid synthesis (SREBP, ACLY, ACC, FASN, and SCD) has been identified as a potential strategy for cancer therapy. By disrupting these enzymes, it may be possible to inhibit tumor growth by interfering with lipid metabolism. Transcription factors, like SREBP play a significant role in regulating fatty acid synthesis which is influenced by circadian clock genes such as BMAL1, REV-ERB and DEC. This suggests a strong connection between fatty acid synthesis and the circadian clock. Therefore, successful combination therapy should target fatty acid synthesis in addition to considering the timing and duration of drug use. Ultimately, personalized chronotherapy can enhance drug efficacy in cancer treatment and achieve treatment goals.
Topics: Humans; Lipid Metabolism; Circadian Clocks; Sterol Regulatory Element Binding Protein 1; Lipid Metabolism Disorders; Neoplasms; Fatty Acids
PubMed: 38189049
DOI: 10.3389/fendo.2023.1292011 -
California Medicine Apr 1971Sphingolipidoses are an heterogeneous group of inherited disorders of lipid metabolism affecting primarily the central nervous system. These disorders occur chiefly in...
Sphingolipidoses are an heterogeneous group of inherited disorders of lipid metabolism affecting primarily the central nervous system. These disorders occur chiefly in the pediatric population, and the degenerative nature of the disease processes is generally characterized by diffuse and progressive involvement of neurones (gray matter) with psychomotor retardation and myoclonus or of fiber tracts (white matter) with weakness and spasticity. Biochemical research has identified the defects in the sphingolipidoses to specific lysosomal enzymes. For example, Niemann-Pick disease lacks sphingomyelinase; Krabbe's disease lacks galactocerebrosidase; Gaucher's disease lacks beta-D-glucosidase; metachromatic leukodystrophy lacks sulfatase; Tay-Sachs disease lacks hexosaminidase A; and generalized gangliosidosis lacks beta-galactosidase. Although there are no currently available modes of rendering corrective therapy in these disorders, a definitive diagnosis is possible both antepartum as well as postpartum. This information provides a sound and accurate basis for genetic counseling.
Topics: Brain; Diffuse Cerebral Sclerosis of Schilder; Gangliosides; Gaucher Disease; Humans; Infant; Lipid Metabolism; Lipid Metabolism, Inborn Errors; Lipidoses; Niemann-Pick Diseases
PubMed: 5551302
DOI: No ID Found -
International Journal of Molecular... Dec 2022Lifestyle changes have led to increased incidence of cardiovascular disease (CVD); therefore, potential targets against CVD should be explored to mitigate its risks.... (Review)
Review
Lifestyle changes have led to increased incidence of cardiovascular disease (CVD); therefore, potential targets against CVD should be explored to mitigate its risks. Adiponectin (APN), an adipokine secreted by adipose tissue, has numerous beneficial effects against CVD related to glucose and lipid metabolism disorders, including regulation of glucose and lipid metabolism, increasing insulin sensitivity, reduction of oxidative stress and inflammation, protection of myocardial cells, and improvement in endothelial cell function. These effects demonstrate the anti-atherosclerotic and antihypertensive properties of APN, which could aid in improving myocardial hypertrophy, and reducing myocardial ischemia/reperfusion (MI/R) injury and myocardial infarction. APN can also be used for diagnosing and predicting heart failure. This review summarizes and discusses the role of APN in the treatment of CVD related to glucose and lipid metabolism disorders, and explores future APN research directions and clinical application prospects. Future studies should elucidate the signaling pathway network of APN cardiovascular protective effects, which will facilitate clinical trials targeting APN for CVD treatment in a clinical setting.
Topics: Humans; Cardiovascular Diseases; Adiponectin; Glucose; Lipid Metabolism; Myocardial Reperfusion Injury; Lipid Metabolism Disorders
PubMed: 36555264
DOI: 10.3390/ijms232415627 -
International Journal of Biological... 2021Glucose and lipids are important nutrients that provide the majority of energy for each organ to maintain homeostasis of the body. With the continuous improvement in... (Review)
Review
Glucose and lipids are important nutrients that provide the majority of energy for each organ to maintain homeostasis of the body. With the continuous improvement in living standards, the incidence of metabolic disorder-associated diseases, such as diabetes, hyperlipidemia, and atherosclerosis, is increasing worldwide. Among them, diabetes, which could be induced by both glucose and lipid metabolic disorders, is one of the five diseases with the highest incidence and mortality worldwide. However, the detailed molecular mechanisms underlying glucose and lipid metabolism disorders and target-organ damage are still not fully defined. MicroRNAs (miRNAs) are small, non-coding, single-stranded RNAs, which usually affect their target mRNAs in the cytoplasm by post-transcriptional regulation. Previously, we have found that miR-320 contributed to glucose and lipid metabolism via different signaling pathways. Most importantly, we identified that nuclear miR-320 mediated diabetes-induced cardiac dysfunction by activating the transcription of fatty acid metabolic genes to cause lipotoxicity in the heart. Here, we reviewed the roles of miR-320 in glucose and lipid metabolism and target-organ damage.
Topics: Biomarkers; Glucose Metabolism Disorders; Humans; Lipid Metabolism Disorders; MicroRNAs
PubMed: 33613101
DOI: 10.7150/ijbs.53419 -
Advances in Experimental Medicine and... 2019Finding new therapeutic targets of glomerulosclerosis treatment is an ongoing quest. Due to a living environment of various stresses and pathological stimuli, podocytes... (Review)
Review
Finding new therapeutic targets of glomerulosclerosis treatment is an ongoing quest. Due to a living environment of various stresses and pathological stimuli, podocytes are prone to injuries; moreover, as a cell without proliferative potential, loss of podocytes is vital in the pathogenesis of glomerulosclerosis. Thus, sufficient understanding of factors and underlying mechanisms of podocyte injury facilitates the advancement of treating and prevention of glomerulosclerosis. The clinical symptom of podocyte injury is proteinuria, sometimes with loss of kidney functions progressing to glomerulosclerosis. Injury-induced changes in podocyte physiology and function are actually not a simple passive process, but a complex interaction of proteins that comprise the anatomical structure of podocytes at molecular levels. This chapter lists several aspects of podocyte injuries along with potential mechanisms, including glucose and lipid metabolism disorder, hypertension, RAS activation, micro-inflammation, immune disorder, and other factors. These aspects are not technically separated items, but intertwined with each other in the pathogenesis of podocyte injuries.
Topics: Glomerulosclerosis, Focal Segmental; Humans; Hypertension; Inflammation; Lipid Metabolism Disorders; Podocytes; Proteinuria
PubMed: 31399967
DOI: 10.1007/978-981-13-8871-2_10 -
Molecular Medicine Reports Jul 2015The association between lipid and bone metabolism has become an increasing focus of interest in recent years, and accumulating evidence has shown that atherosclerosis... (Review)
Review
The association between lipid and bone metabolism has become an increasing focus of interest in recent years, and accumulating evidence has shown that atherosclerosis (AS) and osteoporosis (OP), a disorder of bone metabolism, frequently co-exist. Fat and bone are known to share a common progenitor cell: Multipotent mesenchymal stem cells (MSC) in the bone marrow (BM), which are able to differentiate into various cell phenotypes, including osteoblasts, adipocytes and chondrocytes. Laboratory-based and clinical trials have shown that increasing adipocytes are accompanied by a decrease in bone mineral density (BMD) and bone mass. Statins, lipid-lowering drugs used to treat hyperlipidemia, also provide benefit in the treatment of OP. There is thus evidence that the metabolism of lipids is correlated with that of bone, and that the two are mutually regulated. The present review primarily focuses on the potential association between lipid metabolism disturbance and OP, based on biological metabolism, pathophysiological processes, results from clinical and experimental animal studies, processes involved in the differentiation of adipocytes and osteoblasts, as well as pharmacological treatments of these diseases.
Topics: Adipocytes; Bone Marrow; Bone and Bones; Cell Differentiation; Chondrocytes; Humans; Lipid Metabolism Disorders; Mesenchymal Stem Cells; Osteoblasts; Osteoporosis
PubMed: 25760577
DOI: 10.3892/mmr.2015.3472 -
Hormone Molecular Biology and Clinical... Apr 2016Over the past decades, obesity and its metabolic co-morbidities such as type 2 diabetes (T2D) developed to reach an endemic scale. However, the mechanisms leading to the... (Review)
Review
Over the past decades, obesity and its metabolic co-morbidities such as type 2 diabetes (T2D) developed to reach an endemic scale. However, the mechanisms leading to the development of T2D are still poorly understood. One main predictor for T2D seems to be lipid accumulation in "non-adipose" tissues, best known as ectopic lipid storage. A growing body of data suggests that these lipids may play a role in impairing insulin action in metabolic tissues, such as liver and skeletal muscle. This review aims to discuss recent literature linking ectopic lipid storage and insulin resistance, with emphasis on lipid deposition in skeletal muscle. The link between skeletal muscle lipid content and insulin sensitivity, as well as the mechanisms of lipid-induced insulin resistance and potential therapeutic strategies to alleviate lipotoxic lipid pressure in skeletal muscle will be discussed.
Topics: Adipose Tissue; Animals; Humans; Insulin Resistance; Lipid Metabolism; Lipid Metabolism Disorders; Muscle, Skeletal
PubMed: 26741351
DOI: 10.1515/hmbci-2015-0045 -
EMBO Molecular Medicine Oct 2019The light-sensitive photoreceptors in the retina are extremely metabolically demanding and have the highest density of mitochondria of any cell in the body. Both... (Review)
Review
The light-sensitive photoreceptors in the retina are extremely metabolically demanding and have the highest density of mitochondria of any cell in the body. Both physiological and pathological retinal vascular growth and regression are controlled by photoreceptor energy demands. It is critical to understand the energy demands of photoreceptors and fuel sources supplying them to understand neurovascular diseases. Retinas are very rich in lipids, which are continuously recycled as lipid-rich photoreceptor outer segments are shed and reformed and dietary intake of lipids modulates retinal lipid composition. Lipids (as well as glucose) are fuel substrates for photoreceptor mitochondria. Dyslipidemia contributes to the development and progression of retinal dysfunction in many eye diseases. Here, we review photoreceptor energy demands with a focus on lipid metabolism in retinal neurovascular disorders.
Topics: Animals; Dyslipidemias; Energy Metabolism; Humans; Lipid Metabolism; Metabolic Diseases; Photoreceptor Cells; Retinal Diseases
PubMed: 31486227
DOI: 10.15252/emmm.201910473 -
Current Opinion in Cardiology May 2010In this review, we will highlight recent advances in identifying genes and gene regions responsible for the variation in serum lipid levels. We will also consider the... (Review)
Review
PURPOSE OF REVIEW
In this review, we will highlight recent advances in identifying genes and gene regions responsible for the variation in serum lipid levels. We will also consider the next directions for research based on these advances.
RECENT FINDINGS
Large-scale genome-wide association studies have successfully screened common variants across the genome for association with serum lipids and have generated novel hypotheses about the causes of serum lipid variation.
SUMMARY
Deep sequencing of genome-wide association signals promises to expand the catalogue of variants responsible for serum lipid variation and, with a full catalogue of variants, we may develop a panel of polymorphisms with clinical utility. In parallel, functional exploration of the genome-wide association signals should expand our knowledge of lipoprotein metabolism and generate targets for pharmacologic intervention.
Topics: Genetic Predisposition to Disease; Genetic Variation; Genome-Wide Association Study; Humans; Lipid Metabolism Disorders; Lipids; Pharmacogenetics; Polymorphism, Genetic; Polymorphism, Single Nucleotide; Sequence Analysis, DNA
PubMed: 20224388
DOI: 10.1097/HCO.0b013e328338574d -
Current Opinion in Lipidology Jun 2018Intracellular lipid metabolism is a complex interplay of exogenous lipid handling, trafficking, storage, lipolysis, and export. Recent work has implicated the cellular... (Review)
Review
PURPOSE OF REVIEW
Intracellular lipid metabolism is a complex interplay of exogenous lipid handling, trafficking, storage, lipolysis, and export. Recent work has implicated the cellular degradative process called autophagy in several aspects of lipid metabolism. We will discuss both the classical and novel roles of autophagy and the autophagic machinery in this setting.
RECENT FINDINGS
The delivery of lipid droplets to lysosomes for hydrolysis, named lipophagy, was the first described functional role for autophagy in lipid metabolism. The molecular machinery and regulation of this selective form of macroautophagy is beginning to be discovered and has the potential to shed enormous light on intracellular lipolysis. Yet, the autophagic machinery appears to also be coopted for alternative roles that include interaction with cytosolic lipolysis pathways, supply and expansion of lipid droplets, and lipoprotein trafficking. Additionally, lesser studied forms of autophagy called microautophagy and chaperone-mediated autophagy have distinct roles in lipid handling that also intersect with classical macroautophagy. The integration of current knowledge in these areas into a holistic understanding of intracellular lipid metabolism will be a goal of this review.
SUMMARY
As the field of autophagy has evolved and expanded to include functional roles in various aspects of cellular degradation, so has its role in intracellular lipid metabolism. Understanding the mechanisms underlying these classical and alternative roles of autophagy will not only enhance our knowledge in lipid biology but also provide new avenues of translation to human lipid disorders.
Topics: Animals; Autophagy; Humans; Lipid Droplets; Lipid Metabolism Disorders; Lipolysis; Lipoproteins; Lysosomes; Protein Transport
PubMed: 29601311
DOI: 10.1097/MOL.0000000000000509