scholarly journals Anti-Obesity Effects of Collagen Peptide Derived from Skate (Raja kenojei) Skin Through Regulation of Lipid Metabolism

Marine Drugs ◽  
2018 ◽  
Vol 16 (9) ◽  
pp. 306 ◽  
Author(s):  
Minji Woo ◽  
Yeong Song ◽  
Keon-Hee Kang ◽  
Jeong Noh
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Protein Expression ◽  
The Body ◽  
Chow Diet ◽  
Dependent Manner ◽  
Hepatic Lipid ◽  
Collagen Peptide

This study investigated the anti-obesity effects of collagen peptide derived from skate skin on lipid metabolism in high-fat diet (HFD)-fed mice. All C57BL6/J male mice were fed a HFD with 60% kcal fat except for mice in the normal group which were fed a chow diet. The collagen-fed groups received collagen peptide (1050 Da) orally (100, 200, or 300 mg/kg body weight per day) by gavage, whereas the normal and control groups were given water (n = 9 per group). The body weight gain and visceral adipose tissue weight were lower in the collagen-fed groups than in the control group (p < 0.05). Plasma and hepatic lipid levels were significantly reduced by downregulating the hepatic protein expression levels for fatty acid synthesis (sterol regulatory element binding protein-1 (SREBP-1), fatty acid synthase (FAS), and acetyl-CoA carboxylase (ACC)) and cholesterol synthesis (SREBP-2 and 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR)) and upregulating those for β-oxidation (peroxisome proliferator-activated receptor alpha (PPAR-α) and carnitine palmitoyltransferase 1 (CPT1)) and synthesis of bile acid (cytochrome P450 family 7 subfamily A member 1 (CYP7A1)) (p < 0.05). In the collagen-fed groups, the hepatic protein expression level of phosphorylated 5′ adenosine monophosphate-activated protein kinase (p-AMPK) and plasma adiponectin levels were higher, and the leptin level was lower (p < 0.05). Histological analysis revealed that collagen treatment suppressed hepatic lipid accumulation and reduced the lipid droplet size in the adipose tissue. These effects were increased in a dose-dependent manner. The findings indicated that skate collagen peptide has anti-obesity effects through suppression of fat accumulation and regulation of lipid metabolism.

scholarly journals Perilipin 5 S155 phosphorylation by PKA is required for the control of hepatic lipid metabolism and glycemic control

2020 ◽  
pp. jlr.RA120001126
Author(s):  
Stacey N Keenan ◽  
William DeNardo ◽  
Jieqiong Lou ◽  
Ralf B. Schittenhelm ◽  
Magdalene K. Montgomery ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Glycemic Control ◽  
Fatty Acid Oxidation ◽  
Lipid Droplet ◽  
Critical Role ◽  
The Body ◽  
Acid Oxidation ◽  
Hepatic Lipid Metabolism ◽  
Hepatic Lipid

Perilipin (PLIN) 5 is a lipid droplet-associated protein that coordinates intracellular lipolysis in highly oxidative tissues and is thought to regulate lipid metabolism in response to phosphorylation by protein kinase A (PKA). We sought to identify PKA phosphorylation sites in PLIN5 and assess their functional relevance in cultured cells and the livers of mice. We detected phosphorylation on S155, S161 and S163 of recombinant PLIN5 by PKA in vitro and identified S155 as a functionally important site for lipid metabolism. Expression of phosphorylation-defective PLIN5 S155A in Plin5 null cells resulted in decreased rates of lipolysis and triglyceride-derived fatty acid oxidation compared with cells expressing wildtype PLIN5. These differences in lipid metabolism were not associated with differences in the cellular distribution of PLIN5. Rather, FLIM-FRET analysis of protein-protein interactions showed that PLIN5 S155 phosphorylation regulates PLIN5 interaction with adipose triglyceride lipase (ATGL) at the lipid droplet, but not with the co-activator of ATGL, α-β hydrolase domain-containing 5 (ABHD5). Re-expression of PLIN5 S155A in the liver of Plin5 liver-specific null mice reduced lipolysis when compared to mice with wildtype PLIN5 re-expression, but was not associated with other changes in hepatic lipid metabolism, such as fatty acid oxidation, de novo lipogenesis and triglyceride secretion. Furthermore, glycemic control was impaired in mice with expression of PLIN5 S155A compared with mice expressing PLIN5. Together, these studies demonstrate that PLIN5 S155 is required for PKA-mediated lipolysis and builds on the body of evidence demonstrating a critical role for PLIN5 in coordinating lipid and glucose metabolism

scholarly journals Regulatory Effects of Skate Skin-Derived Collagen Peptides with Different Molecular Weights on Lipid Metabolism in the Liver and Adipose Tissue

Biomedicines ◽  
2020 ◽  
Vol 8 (7) ◽  
pp. 187
Author(s):  
Minji Woo ◽  
Jeong Sook Noh
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Control Group ◽  
Water Control ◽  
Tissue Mass ◽  
Hepatic Lipid ◽  
Molecular Weights ◽  
Hepatic Lipid Accumulation ◽  
Collagen Peptide ◽  
Skin Collagen

This study investigated the effects of skate skin collagen peptide (SSCP) with different molecular weights (MWs) on the lipid metabolism in the liver and adipose tissue. Male db/db mice were orally administered with water (control group) or low SSCP (LCP group) or high SSCP (HCP group) MW for 8 weeks whereas male m/m mice were used for comparison (normal group) (n = 10 each group). Compared to the control group, the LCP and HCP groups had lower adipose tissue mass, plasma and hepatic lipid concentrations, and plasma leptin levels (p < 0.05). Protein expression levels of lipogenesis-related protein were reduced in both liver and adipose tissues of SSCP-fed groups whereas those for lipolysis were elevated (p < 0.05). In particular, the LCP had the higher effects relative to the HCP. The above results were supported by histological analysis, revealing that SSCP administration decreased the size of adipose droplets and suppressed hepatic lipid accumulation. Our results showed that SSCP has potential antiobesity properties through the improvement of lipid metabolism in the liver and adipose tissue; in particular, the lower MW of collagen peptide had the greater effects.

Lipid metabolism during lactation: a review of adipose tissue-liver interactions and the development of fatty liver

2005 ◽  
Vol 72 (4) ◽  
pp. 460-469 ◽  
Author(s):  
Richard G Vernon
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Negative Energy ◽  
The Body ◽  
Unesterified Fatty Acid ◽  
Adipose Tissue Depots

Fatty acids are the major source of energy for most tissues during periods of negative energy balance; however, fatty acids can, in some circumstances, have pathological effects. Fatty acids are stored as triacylglycerols (TAG), mostly in the various adipose tissue depots of the body. However, if blood unesterified fatty acid (NEFA) levels are elevated for prolonged periods, as may occur during lactation or obesity, TAG can accumulate in other tissues including liver and muscle cells (myocytes), and this can have pathological consequences such as the development of ketosis (Grummer, 1993; Drackley et al. 2001) or type 2 diabetes (Boden & Shulman, 2002; McGarry, 2002).

scholarly journals Hepatic PKA inhibition accelerates the lipid accumulation in liver

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Jining Yang ◽  
Xiaoying Zhang ◽  
Long Yi ◽  
Ling Yang ◽  
Wei Eric Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Rna Sequencing ◽  
Lipid Accumulation ◽  
The Body ◽  
Chow Diet ◽  
Alcoholic Fatty Liver ◽  
Liver Index ◽  
Triglyceride Accumulation ◽  
And Control

Abstract Background/aims Liver lipid accumulation induced by high-fat diet (HFD) is an early onset process of non-alcoholic fatty liver diseases (NAFLD). Protein kinase A (PKA) is known to be involved in hepatic lipid metabolism. However, the role of PKA in NAFLD has not been well tested in vivo due to the lack of optimal PKA deficient mouse model. Methods A novel PKA-specific inhibitor gene was conditionally overexpressed in mouse (PKAi mouse) liver using LoxP/Cre system. PKA activity in the liver extract was measured with a commercial assay kit. The PKAi and control mice of 8-week age, were subjected to HFD or chow diet (CD) for 2 months. Body weight, liver index, and triglyceride in the liver were measured. RNA sequencing was performed for the liver tissues and analyzed with Gene Ontology (GO) and pathway enrichment. Results PKAi-GFP protein was overexpressed in the liver and the PKA activation was significantly inhibited in the liver of PKAi mouse. When fed with CD, RNA sequencing revealed 56 up-regulated and 51 down-regulated genes in PKAi mice compared with control mice, which were mainly involved in lipid metabolism though no significant differences in the body weight, liver index, triglyceride accumulation were observed between PKAi and control mice. However, when fed with HFD for 2 months, the liver was enlarged more, and the accumulation of triglyceride in the liver was more severe in PKAi mice. When comparing the transcriptomes of CD-fed and HFD-fed control mice, GO enrichment showed that the genes down-regulated by HFD were mainly enriched in immune-related GO terms, and up-regulated genes were enriched in metabolism. When comparing the transcriptomes of CD-fed and HFD-fed PKAi mice, GO analysis showed that the down-regulated genes were enriched in metabolism, while the up-regulated genes were clustered in ER stress-related pathways. When comparing HFD-fed PKAi and HFD-fed control mice, the genes with lower expression level in PKAi mice were enriched in the lipoprotein synthesis, which might explain that more TG is accumulated in PKAi liver after HFD feeding. Conclusions Reduced PKA activity could be a factor promoting the TG accumulation in the liver and the development of NAFLD.

scholarly journals D-Mannitol Induces a Brown Fat-like Phenotype via a β3-Adrenergic Receptor-Dependent Mechanism

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 768
Author(s):  
Hui-Jeon Jeon ◽  
Dong Kyu Choi ◽  
JaeHeon Choi ◽  
Seul Lee ◽  
Heejin Lee ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Protein Kinase ◽  
White Adipose Tissue ◽  
Adrenergic Receptor ◽  
Uncoupling Protein ◽  
The Body ◽  
Brown Fat ◽  
White Adipocytes

The presence of brown adipocytes within white adipose tissue is associated with phenotypes that exhibit improved metabolism and proper body weight maintenance. Therefore, a variety of dietary agents that facilitate the browning of white adipocytes have been investigated. In this study, we screened a natural product library comprising 133 compounds with the potential to promote the browning of white adipocytes, and found that D-mannitol induces the browning of 3T3-L1 adipocytes by enhancing the expression of brown fat-specific genes and proteins, and upregulating lipid metabolism markers. D-mannitol also increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase 1 (ACC), suggesting a possible role in lipolysis and fat oxidation. Moreover, an increase in the expression of genes associated with D-mannitol-induced browning was strongly correlated with the activation of the β3-adrenergic receptor as well as AMPK, protein kinase A (PKA), and PPARγ coactivator 1α (PGC1α). D-mannitol effectively reduced the body weight of mice fed a high-fat diet, and increased the expression of β1-oxidation and energy expenditure markers, such as Cidea, carnitine palmityl transferase 1 (CPT1), uncoupling protein 1 (UCP1), PGC1α, and acyl-coenzyme A oxidase (ACOX1) in the inguinal white adipose tissue. Our findings suggest that D-mannitol plays a dual regulatory role by inducing the generation of a brown fat-like phenotype and enhancing lipid metabolism. These results indicate that D-mannitol can function as an anti-obesity supplement.

Effects of Nannochloropsis Fed on Serum and Tissue Lipids Metabolism in Obese Offspring of Overfed Dams

2019 ◽  
Vol 15 (1) ◽  
pp. 72-86
Author(s):  
Soraya Bendimerad-Benmokhtar ◽  
Samira Bouanane ◽  
Hafida Merzouk ◽  
Fatima Zohra Baba Ahmed ◽  
Asme Bendaoud
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Maternal Diet ◽  
Control Diet ◽  
Visceral Obesity ◽  
Female Offspring ◽  
The Body ◽  
Cafeteria Diet ◽  
Lipids Metabolism

Background: The present work aims at determining the effects of maternal-diet-induced obesity on offspring metabolism. The short-term of a marine microalgae diet and its effects on lipids metabolism was investigated. </P><P> Method: Before gestation, some rats are fed control diet and others cafeteria diet. Moreover, two groups of dams were fed standard and cafeteria diets, and two other groups were fed the same diets but containing 10% of microalgae. This feeding started at gestation, and continued throughout parturition, lactation until their offspring&#039;s weaning age. </P><P> Results: Cafeteria diet was shown to increase the body weight and visceral obesity, with aberration in lipid metabolism. The results obtained show that the microalgae diet supplement induces a significant decrease in the maternal body weight and relative adipose tissue weight, plasma glucose and lipid levels, liver-triglyceride (TG) and adipose tissue-TG at parturition and at the end of lactation. Also, the addition of the microalgae in both males and female offspring fed dams at birth and weaning showed significant decrease in body weight, liver-TG whereas significant increase in TG-HDL. </P><P> Conclusion: In the end, it was noted that the incorporation of 10% of microalgae has a beneficial effect on body weight and lipid metabolism.

scholarly journals Thermoneutrality Inhibits Thermogenic Markers and Exacerbates Nonalcoholic Fatty Liver in Mice (P21-068-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lei Hao ◽  
Md Shahjalal Hossain Khan ◽  
Yujiao Zu ◽  
Jie Liu ◽  
Shu Wang
Keyword(s):  
Drinking Water ◽  
Body Weight ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Chow Diet ◽  
Nonalcoholic Fatty Liver ◽  
Brown Adipose

Abstract Objectives Nonalcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease, affecting more than a third of the US population and 25% of the global population. In this study, we investigated whether manipulation of brown adipose tissue (BAT) activity via housing C57BL/6 J mice under two different housing temperatures (22°C vs 27°C) influences the development of NAFLD. Methods Male C57BL/6 J mice were randomly allocated to 4 groups (8 mice/group). Briefly, mice housed at the standard temperature (ST) (22°C) or thermoneutral temperature (TT) (27°C) were fed either a control chow diet (CHD) (Picolab rodent diet 20, LabDiet) with a regular drinking water or an “fast food” diet (FFD) (Research Diets, D12079B) plus fructose 23.1 g/L and glucose 18.9 g/L added to the drinking water for 10 weeks. Results Mice under TT had significant less food intake compared to their counter partners under ST, regardless of diets. Mice exposed to TT and fed FFD had the highest body weight and plasma leptin level among all groups. For mice fed CHD, mice at TT did not present hepatic steatosis although they slightly gained more body weight compared to mice at ST. For mice fed FFD, thermoneutral housing mice had greater liver weight, liver triglyceride, and exacerbated hepatic steatosis compared to the standard housing mice. Moreover, for mice fed FFD, TT compared to ST had significantly elevated expression of fatty acid synthase, sterol regulatory element-binding transcription factor 1, fatty acid translocase, and monocyte chemoattractant protein-1 in liver. By contrast, TT did not change expression of above genes in mice fed CHD. Furthermore, thermoneutrally housed mice displayed a decrease in gene expression of thermogenic markers, such as uncoupling protein 1, elongation of very long chain fatty acids 3, and cell death-inducing DNA fragmentation factor alpha-like effector A in BAT and inguinal white adipose tissue (WAT). Conclusions Thermoneutrality inhibits expression of thermogenic markers in both BAT and WAT, which correlated to exacerbated NAFLD in mice. Our data indicate that activating BAT and/or promoting WAT browning may represent a potential strategy for the management of NAFLD. Funding Sources The College of Human Sciences of Texas Tech University; the National Center for Complementary & Integrative Health.

scholarly journals Chlorogenic acid and caffeine in combination inhibit fat accumulation by regulating hepatic lipid metabolism-related enzymes in mice

2014 ◽  
Vol 112 (6) ◽  
pp. 1034-1040 ◽  
Author(s):  
Guodong Zheng ◽  
Yangyang Qiu ◽  
Qing-Feng Zhang ◽  
Dongming Li
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Protein Expression ◽  
Chlorogenic Acid ◽  
Health Concern ◽  
Hepatic Lipid Metabolism ◽  
Fat Accumulation ◽  
Expression Levels ◽  
Hepatic Lipid ◽  
Mrna And Protein Expression

Obesity has become a public health concern due to its positive association with the incidence of many diseases, and coffee components including chlorogenic acid (CGA) and caffeine have been demonstrated to play roles in the suppression of fat accumulation. To investigate the mechanism by which CGA and caffeine regulate lipid metabolism, in the present study, forty mice were randomly assigned to four groups and fed diets containing no CGA or caffeine, CGA, caffeine, or CGA+caffeine for 24 weeks. Body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters were measured, and the activities and mRNA and protein expression of lipid metabolism-related enzymes were analysed. There was a decrease in the body weight and IPAT weight of mice fed the CGA+caffeine diet. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA+caffeine diet. The activities of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO) were increased in mice fed the caffeine and CGA+caffeine diets, while the activity of fatty acid synthase (FAS) was suppressed in those fed the CGA+caffeine diet. The mRNA expression levels of AMP-activated protein kinase (AMPK),CATandACOwere considerably up-regulated in mice fed the CGA+caffeine diet, while those ofPPARγ2were down-regulated. The protein expression levels of AMPK were increased and those of FAS were decreased in mice fed the CGA+caffeine diet. These results indicate that CGA+caffeine suppresses fat accumulation and body weight gain by regulating the activities and mRNA and protein expression levels of hepatic lipid metabolism-related enzymes and that these effects are stronger than those exerted by CGA and caffeine individually.

Antihyperlipidemic and Hepatoprotective Properties of Vitamin B6 Supplementation in Rats with High-Fat Diet-Induced Hyperlipidemia

2021 ◽  
Vol 21 ◽  
Author(s):  
Qian Zhang ◽  
Da-long Zhang ◽  
Xiao-li Zhou ◽  
Qian Li ◽  
Ning He ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Protein Expression ◽  
High Fat Diet ◽  
Vitamin B6 ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Atherogenic Index ◽  
High Fat ◽  
Hepatic Lipid

Background: The incidence and mortality of hyperlipidemia are increasing year by year, showing a younger trend. At present, the treatment of hyperlipidemia is mainly dependent on western medicine, but its side effects on liver and kidney function are common in clinics. Therefore, it is necessary to study the treatment of hyperlipidemia by augmenting effective dietary nutrition supplements. Vitamin B6 (VitB6), as an essential cofactor for enzymes, participates in lipid metabolism. The effects of VitB6 on hyperlipidemia, however, have not been reported until now. Aim: The present study was to investigate the influence of VitB6 on hepatic lipid metabolism in hyperlipidaemia rats induced by a high-fat diet (HFD). Methods: Male Sprague-Dawley rats were kept on HFD for two weeks to establish the hyperlipidemia model. The rats in low-dosage and high-dosage groups were received 2.00 and 3.00 mg/kg/day of VitB6 for eight weeks, respectively. Results: The results showed that both doses of VitB6 reduced HFD-induced hepatic low-density lipoprotein cholesterol (LDL-C); decreased blood cholesterol (TC), triglycerides, LDL-C, atherogenic index (AI), atherogenic index of plasma (AIP), apolipoprotein B (ApoB) and ApoB/apolipoprotein A-1(ApoA1) ratio; increased liver high-density lipoprotein cholesterol (HDL-C) and serum ApoA1; reduced hepatic steatosis and triglyceride accumulation, lowered fat storage, and recovered heart/body and brain/body ratio to a normal level. In addition, VitB6 supplementation markedly decreased HMGR level, increased the mRNA abundance of LDLR and CYP7A1, and protein expression of SIRT1, following the downregulation of SREBP-1 and PPARγ protein expression in the liver of hyperlipidemia rats. Conclusion: In summary, oral VitB6 supplementation can ameliorate HFD-induced hepatic lipid accumulation and dyslipidemia in SD rats by inhibiting fatty acid and cholesterol synthesis, promoting fatty acid decomposition and cholesterol transport.

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