scholarly journals Mechanism of liver lipid accumulation in low protein diet feeding. III. Triglyceride release and fatty acid oxidation by the perfused liver of rats fed a low protein diet.

1977 ◽  
Vol 41 (8) ◽  
pp. 1435-1441
Author(s):  
Kazumi YAGASAKI ◽  
Masao KAMETAKA
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Accumulation ◽  
Liver Lipid ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Acid Oxidation ◽  
Perfused Liver ◽  
Low Protein

scholarly journals MON-672 Progesterone Receptor Membrane Component 1 Suppresses Lipid Accumulation and Lipotoxicity in Animal Model of Diabetic Cardiomyopathy (DCM)

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sang R Lee ◽  
Eui-ju Hong
Keyword(s):  
Fatty Acid ◽  
Progesterone Receptor ◽  
Fatty Acid Oxidation ◽  
Diabetic Cardiomyopathy ◽  
Mitochondrial Respiration ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Membrane Component

Abstract Diabetic cardiomyopathy (DCM) is one of the complications triggered by type II diabetes (T2D) (1). When free fatty acids (FFA) are abundant in insulin resistant pre-diabetic patients because of adipose lipolysis, FFA tends to move toward heart (2). Lipid accumulation can cause cardiac lipotoxicity and exacerbate DCM (3). In previous study, Pgrmc1 has been identified to associate with fatty acid synthesis (4). Therefore, we assumed that Pgrmc1 will associate with DCM. By feeding high-fat diet for 8 weeks and injecting streptozotocin (30mg/kg), T2D and DCM were induced. The lipid accumulation was exacerbated in T2D-induced Pgrmc1 KO heart, and FFA level was also high. Levels of lipid metabolic genes showed the tendency for lipid accumulation and lipotoxicity, and glycolysis was induced in T2D-induced Pgrmc1 KO heart. Though glycolysis presents higher efficiency for energy production in cardiomyopathy (5), it did not compensate the impairment of mitochondrial respiration in Pgrmc1 KO heart. High-fat diet and streptozotocin could not be the interfering factors, because suppression of fatty acid oxidation, induction of glycolysis, and impairment of mitochondrial respiration were observed similarly in post-prandial mice which were fed with normal chow. Insulin was excluded for interfering factor as cell line with serum starvation showed mitochondrial suppression and glycolytic induction in flux analyzer analysis in Pgrmc1 knockdown. Conversely, induction of fatty acid oxidation and suppression of glycolysis were observed in 72 h fasting of Pgrmc1 KO heart, suggesting the nutrition is closely associated with the metabolic modulation of Pgrmc1 on heart. This metabolic phenotype of Pgrmc1 KO heart consequently exacerbated DCM by showing high levels of fibrosis, inflammation, endoplasmic reticulum stress, and oxidative stress. References: (1) Jia G, Hill MA, Sowers JR. Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity. Circulation research. 2018;122:624-38. (2) Noll C, Carpentier AC. Dietary fatty acid metabolism in prediabetes. Current opinion in lipidology. 2017;28:1-10. (3) Goldberg IJ, Trent CM, Schulze PC. Lipid metabolism and toxicity in the heart. Cell metabolism. 2012;15:805-12. (4) Lee SR, Kwon SW, Kaya P, Lee YH, Lee JG, Kim G, et al. Loss of progesterone receptor membrane component 1 promotes hepatic steatosis via the induced de novo lipogenesis. Scientific reports. 2018;8:15711. (5) Nagoshi T, Yoshimura M, Rosano GM, Lopaschuk GD, Mochizuki S. Optimization of cardiac metabolism in heart failure. Current pharmaceutical design. 2011;17:3846-53.

Kaempferol Isolated from Nelumbo nucifera Inhibits Lipid Accumulation and Increases Fatty Acid Oxidation Signaling in Adipocytes

2015 ◽  
Vol 18 (12) ◽  
pp. 1363-1370 ◽  
Author(s):  
Bonggi Lee ◽  
Misung Kwon ◽  
Jae Sue Choi ◽  
Hyoung Oh Jeong ◽  
Hae Young Chung ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Accumulation ◽  
Nelumbo Nucifera ◽  
Acid Oxidation

scholarly journals Berberine Reduces Lipid Accumulation by Promoting Fatty Acid Oxidation in Renal Tubular Epithelial Cells of the Diabetic Kidney

2022 ◽  
Vol 12 ◽  
Author(s):  
Qingfeng Rong ◽  
Baosheng Han ◽  
Yafeng Li ◽  
Haizhen Yin ◽  
Jing Li ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Epithelial Cells ◽  
Fatty Acid Oxidation ◽  
High Glucose ◽  
Lipid Accumulation ◽  
Diabetic Kidney Disease ◽  
Acid Oxidation ◽  
Tubular Epithelial Cells ◽  
Diabetic Kidney ◽  
Renal Tubular

Abnormal lipid metabolism in renal tubular epithelial cells contributes to renal lipid accumulation and disturbed mitochondrial bioenergetics which are important in diabetic kidney disease. Berberine, the major active constituent of Rhizoma coptidis and Cortex phellodendri, is involved in regulating glucose and lipid metabolism. The present study aimed to investigate the protective effects of berberine on lipid accumulation in tubular epithelial cells of diabetic kidney disease. We treated type 2 diabetic db/db mice with berberine (300 mg/kg) for 12 weeks. Berberine treatment improved the physical and biochemical parameters of the db/db mice compared with db/m mice. In addition, berberine decreased intracellular lipid accumulation and increased the expression of fatty acid oxidation enzymes CPT1, ACOX1 and PPAR-α in tubular epithelial cells of db/db mice. The mitochondrial morphology, mitochondrial membrane potential, cytochrome c oxidase activity, mitochondrial reactive oxygen species, and mitochondrial ATP production in db/db mice kidneys were significantly improved by berberine. Berberine intervention activated the AMPK pathway and increased the level of PGC-1α. In vitro berberine suppressed high glucose-induced lipid accumulation and reversed high glucose-induced reduction of fatty acid oxidation enzymes in HK-2 cells. Importantly, in HK-2 cells, berberine treatment blocked the change in metabolism from fatty acid oxidation to glycolysis under high glucose condition. Moreover, berberine restored high glucose-induced dysfunctional mitochondria. These data suggested that berberine alleviates diabetic renal tubulointerstitial injury through improving high glucose-induced reduction of fatty acid oxidation, alleviates lipid deposition, and protect mitochondria in tubular epithelial cells.

Low-protein diet during gestation and lactation increases hepatic lipid accumulation through autophagy and histone deacetylase

2020 ◽  
Vol 319 (1) ◽  
pp. E11-E25
Author(s):  
Huan Wang ◽  
Guanying Bianca Xu ◽  
Diego Hernández-Saavedra ◽  
Hong Chen ◽  
Yuan-Xiang Pan
Keyword(s):  
Amino Acid ◽  
Histone Deacetylase ◽  
Lipid Accumulation ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Density ◽  
Hepatic Lipid ◽  
Low Protein ◽  
Triglyceride Accumulation ◽  
Autophagic Degradation

The present study examined the mechanism of a low-protein (LP) diet on hepatic lipid metabolism during gestation and lactation. Timed-pregnant Sprague-Dawley rats were fed a control or an LP diet during gestation and lactation. LP dams had increased hepatic triglyceride accumulation and a significantly higher aspartate/alanine transaminase ratio, accompanied by a decrease in the circulating very low-density/low-density lipoprotein ratio. Microtubule-associated protein 1 light-chain 3β (LC3B) expression was stimulated in LP dams along with increased histone acetylation. LP diet induced colocalization of the LC3 binding motif interacting proteins apolipoprotein B (APOB) or microsomal triglyceride transfer protein (MTTP) with LC3B, suggesting autophagic degradation. Histone deacetylase 3 (HDAC3) is found necessary to prevent lipid accumulation in response to amino acid deprivation in HepG2 cells. LC3B-mediated APOB protein degradation is related to increases in lipid accumulation. HDAC3 regulated LC3B-induced lipid accumulation potentially through autophagic degradation of APOB and MTTP in response to amino acid limitation caused by a low-protein diet.

FP384EFFECT OF OMEGA-3 FATTY ACID AND MENAQUINONE-7 ON OSTEOPENIA AND SARCOPENIA IN ADENINE AND LOW PROTEIN DIET INDUCED UREMIC RATS

2018 ◽  
Vol 33 (suppl_1) ◽  
pp. i162-i163
Author(s):  
SuMi Lee ◽  
Eu Gene Jeong ◽  
Sung Hyun Son ◽  
Hyuck Jae Choi ◽  
Young Ki Son ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Omega 3 ◽  
Omega 3 Fatty Acid ◽  
Low Protein
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