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Endocrine, Metabolic & Immune Disorders... 2022Lipid metabolism disorder plays a fundamental role in the pathogenesis of atherosclerosis. As the largest metabolic organ of the human body, the liver has a key role in... (Review)
Review
Lipid metabolism disorder plays a fundamental role in the pathogenesis of atherosclerosis. As the largest metabolic organ of the human body, the liver has a key role in lipid metabolism by influencing fat production, fat decomposition, and the intake and secretion of serum lipoproteins. Numerous clinical and experimental studies have indicated that the dysfunction of hepatic lipid metabolism is closely related to the onset of atherosclerosis. However, the identity and functional role of hepatic lipid metabolism responsible for these associations remain unknown. This review presented that cholesterol synthesis, cholesterol transport, and the metabolism of triglycerides, lipoproteins, and fatty acids are all associated with hepatic lipid metabolism and atherosclerosis. Moreover, the roles of gut microbiota, inflammatory response, and oxidative stress in the pathological association between hepatic lipid metabolism and atherosclerosis are also discussed. This significant evidence strongly supports that hepatic lipid metabolism disorders may increase the risk of atherosclerosis.
Topics: Atherosclerosis; Cholesterol; Humans; Lipid Metabolism; Lipid Metabolism Disorders; Lipoproteins; Liver
PubMed: 34931971
DOI: 10.2174/1871530322666211220110810 -
Biomedicine & Pharmacotherapy =... Oct 2023Lipid metabolism is a complex process that maintains the normal physiological function of the human body. The disorder of lipid metabolism has been implicated in various... (Review)
Review
Lipid metabolism is a complex process that maintains the normal physiological function of the human body. The disorder of lipid metabolism has been implicated in various human diseases, such as cardiovascular diseases and bone diseases. Intervertebral disc degeneration (IDD), an age-related degenerative disease in the musculoskeletal system, is characterized by high morbidity, high treatment cost, and chronic recurrence. Lipid metabolism disorder may promote the pathogenesis of IDD, and the potential mechanisms are complex. Leptin, resistin, nicotinamide phosphoribosyltransferase (NAMPT), fatty acids, and cholesterol may promote the pathogenesis of IDD, while lipocalin, adiponectin, and progranulin (PGRN) exhibit protective activity against IDD development. Lipid metabolism disorder contributes to extracellular matrix (ECM) degradation, cell apoptosis, and cartilage calcification in the intervertebral discs (IVDs) by activating inflammatory responses, endoplasmic reticulum (ER) stress, and oxidative stress and inhibiting autophagy. Several lines of agents have been developed to target lipid metabolism disorder. Inhibition of lipid metabolism disorder may be an effective strategy for the therapeutic management of IDD. However, an in-depth understanding of the molecular mechanism of lipid metabolism disorder in promoting IDD development is still needed.
Topics: Humans; Intervertebral Disc Degeneration; Lipid Metabolism; Lipid Metabolism Disorders; Adiponectin; Apoptosis
PubMed: 37651799
DOI: 10.1016/j.biopha.2023.115401 -
Nutrients Jan 2020Menopause is clinically diagnosed as a condition when a woman has not menstruated for one year. During the menopausal transition period, there is an emergence of various... (Review)
Review
Menopause is clinically diagnosed as a condition when a woman has not menstruated for one year. During the menopausal transition period, there is an emergence of various lipid metabolic disorders due to hormonal changes, such as decreased levels of estrogens and increased levels of circulating androgens; these may lead to the development of metabolic syndromes including cardiovascular diseases and type 2 diabetes. Dysregulation of lipid metabolism affects the body fat mass, fat-free mass, fatty acid metabolism, and various aspects of energy metabolism, such as basal metabolic ratio, adiposity, and obesity. Moreover, menopause is also associated with alterations in the levels of various lipids circulating in the blood, such as lipoproteins, apolipoproteins, low-density lipoproteins (LDLs), high-density lipoproteins (HDL) and triacylglycerol (TG). Alterations in lipid metabolism and excessive adipose tissue play a key role in the synthesis of excess fatty acids, adipocytokines, proinflammatory cytokines, and reactive oxygen species, which cause lipid peroxidation and result in the development of insulin resistance, abdominal adiposity, and dyslipidemia. This review discusses dietary recommendations and beneficial compounds, such as vitamin D, omega-3 fatty acids, antioxidants, phytochemicals-and their food sources-to aid the management of abnormal lipid metabolism in postmenopausal women.
Topics: Adult; Aged; Estrogens; Fatty Acids, Omega-3; Female; Humans; Lipid Metabolism; Lipid Metabolism Disorders; Menopause; Middle Aged; Obesity; Phytochemicals; Postmenopause; Probiotics; Vitamin D
PubMed: 31941004
DOI: 10.3390/nu12010202 -
Frontiers in Endocrinology 2024Diabetic kidney disease (DKD), a significant complication associated with diabetes mellitus, presents limited treatment options. The progression of DKD is marked by... (Review)
Review
Diabetic kidney disease (DKD), a significant complication associated with diabetes mellitus, presents limited treatment options. The progression of DKD is marked by substantial lipid disturbances, including alterations in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids (BAs). Altered lipid metabolism serves as a crucial pathogenic mechanism in DKD, potentially intertwined with cellular ferroptosis, lipophagy, lipid metabolism reprogramming, and immune modulation of gut microbiota (thus impacting the liver-kidney axis). The elucidation of these mechanisms opens new potential therapeutic pathways for DKD management. This research explores the link between lipid metabolism disruptions and DKD onset.
Topics: Humans; Diabetic Nephropathies; Lipid Metabolism; Animals; Lipid Metabolism Disorders; Gastrointestinal Microbiome
PubMed: 38742197
DOI: 10.3389/fendo.2024.1336402 -
DNA and Cell Biology Dec 2017The present review provides a summary of recent evidence of sortilin expression, function, and regulation and its implications in lipid metabolism and development of... (Review)
Review
The present review provides a summary of recent evidence of sortilin expression, function, and regulation and its implications in lipid metabolism and development of lipid disorder diseases. As a member of the vacuolar protein sorting 10 protein (Vps10p) receptor family, sortilin mediates intracellular trafficking of diverse endogenous or exogenous protein substrates between the trans-Golgi network (TGN) and plasma membrane compartments. Recent studies reveal that sortilin regulates the expression of lipid genes, plasma lipid level, and the development of lipid disorder diseases. Sortilin promotes atherogenesis by regulating hepatic very low density lipoprotein (VLDL) secretion and plasma lipid level and subsequently macrophage lipid accumulation. Sortilin deficiency is caused by accelerated proteasome degradation under insulin resistance conditions and is thereby implicated in the hyperlipidemia of type 2 diabetes mellitus (T2DM). Sortilin facilitates hepatic cholesterol accumulation by inhibiting hepatic cholesterol catabolism, which promotes the development of nonalcoholic fatty liver disease (NAFLD). Sortilin plays an important role in lipid metabolism and represents a promising therapeutic target for lipid disorder diseases.
Topics: Adaptor Proteins, Vesicular Transport; Animals; Atherosclerosis; Diabetes Mellitus, Type 2; Dyslipidemias; Humans; Lipid Metabolism; Lipid Metabolism Disorders; Mice; Non-alcoholic Fatty Liver Disease
PubMed: 28945101
DOI: 10.1089/dna.2017.3853 -
Nutrients Dec 2021Aging women experience hormonal changes, such as decreased estrogen and increased circulating androgen, due to natural or surgical menopause. These hormonal changes make... (Review)
Review
Aging women experience hormonal changes, such as decreased estrogen and increased circulating androgen, due to natural or surgical menopause. These hormonal changes make postmenopausal women vulnerable to body composition changes, muscle loss, and abdominal obesity; with a sedentary lifestyle, these changes affect overall energy expenditure and basal metabolic rate. In addition, fat redistribution due to hormonal changes leads to changes in body shape. In particular, increased bone marrow-derived adipocytes due to estrogen loss contribute to increased visceral fat in postmenopausal women. Enhanced visceral fat lipolysis by adipose tissue lipoprotein lipase triggers the production of excessive free fatty acids, causing insulin resistance and metabolic diseases. Because genes involved in β-oxidation are downregulated by estradiol loss, excess free fatty acids produced by lipolysis of visceral fat cannot be used appropriately as an energy source through β-oxidation. Moreover, aged women show increased adipogenesis due to upregulated expression of genes related to fat accumulation. As a result, the catabolism of ATP production associated with β-oxidation decreases, and metabolism associated with lipid synthesis increases. This review describes the changes in energy metabolism and lipid metabolic abnormalities that are the background of weight gain in postmenopausal women.
Topics: Adipogenesis; Aged; Body Composition; Energy Metabolism; Estradiol; Estrogens; Fatty Acids, Nonesterified; Female; Humans; Insulin Resistance; Intra-Abdominal Fat; Lipid Metabolism; Lipid Metabolism Disorders; Lipolysis; Lipoprotein Lipase; Middle Aged; Muscle, Skeletal; Obesity, Abdominal; Oxidation-Reduction; Postmenopause
PubMed: 34960109
DOI: 10.3390/nu13124556 -
Circulation Research Feb 2021Lipid uptake and metabolism are central to the function of organs such as heart, skeletal muscle, and adipose tissue. Although most heart energy derives from fatty acids... (Review)
Review
Lipid uptake and metabolism are central to the function of organs such as heart, skeletal muscle, and adipose tissue. Although most heart energy derives from fatty acids (FAs), excess lipid accumulation can cause cardiomyopathy. Similarly, high delivery of cholesterol can initiate coronary artery atherosclerosis. Hearts and arteries-unlike liver and adrenals-have nonfenestrated capillaries and lipid accumulation in both health and disease requires lipid movement from the circulation across the endothelial barrier. This review summarizes recent in vitro and in vivo findings on the importance of endothelial cell receptors and uptake pathways in regulating FAs and cholesterol uptake in normal physiology and cardiovascular disease. We highlight clinical and experimental data on the roles of ECs in lipid supply to tissues, heart, and arterial wall in particular, and how this affects organ metabolism and function. Models of FA uptake into ECs suggest that receptor-mediated uptake predominates at low FA concentrations, such as during fasting, whereas FA uptake during lipolysis of chylomicrons may involve paracellular movement. Similarly, in the setting of an intact arterial endothelial layer, recent and historic data support a role for receptor-mediated processes in the movement of lipoproteins into the subarterial space. We conclude with thoughts on the need to better understand endothelial lipid transfer for fuller comprehension of the pathophysiology of hyperlipidemia, and lipotoxic diseases such as some forms of cardiomyopathy and atherosclerosis.
Topics: Animals; CD36 Antigens; Cholesterol; Chylomicrons; Endothelial Cells; Fatty Acid Transport Proteins; Fatty Acids; Humans; Lipid Metabolism Disorders; Lipolysis; Particle Size; Transcytosis
PubMed: 33539224
DOI: 10.1161/CIRCRESAHA.120.318003 -
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... 2019Since the lipid nephrotoxicity hypothesis was proposed in 1982, increasing evidence has supported the hypothesis that lipid abnormalities contributed to the progression...
Since the lipid nephrotoxicity hypothesis was proposed in 1982, increasing evidence has supported the hypothesis that lipid abnormalities contributed to the progression of glomerulosclerosis. In this chapter, we will discuss the general promises of the original hypothesis, focusing especially on the role of lipids and metabolic inflammation accompanying CKD in renal fibrosis and potential new strategies of prevention.
Topics: Disease Progression; Fibrosis; Humans; Inflammation; Kidney Diseases; Lipid Metabolism Disorders; Lipids
PubMed: 31399983
DOI: 10.1007/978-981-13-8871-2_26 -
The American Journal of Medicine Feb 2022
Topics: Adult; Benzoxazoles; Blood Glucose; Butyrates; Diabetes Mellitus, Type 2; Diet, Fat-Restricted; Humans; Hyperlipidemias; Hypertriglyceridemia; Hypolipidemic Agents; Insulin; Lipid Metabolism Disorders; Male; Retinal Diseases; Xanthomatosis
PubMed: 34655537
DOI: 10.1016/j.amjmed.2021.09.011