Responses of energy homeostasis and lipid metabolism in Penaeus vannamei exposed to ammonia stress

Maternal malnutrition in critical periods of development increases the risk of developing short- and long-term diseases in the offspring. The alterations induced by this nutritional programming in the hypothalamus of the offspring are of special relevance due to its role in energy homeostasis, especially in the endocannabinoid system (ECS), which is involved in metabolic functions. Since astrocytes are essential for neuronal energy efficiency and are implicated in brain endocannabinoid signaling, here we have used a rat model to investigate whether a moderate caloric restriction (R) spanning from two weeks prior to the start of gestation to its end induced changes in offspring hypothalamic (a) ECS, (b) lipid metabolism (LM) and/or (c) hypothalamic astrocytes. Monitorization was performed by analyzing both the gene and protein expression of proteins involved in LM and ECS signaling. Offspring born from caloric-restricted mothers presented hypothalamic alterations in both the main enzymes involved in LM and endocannabinoids synthesis/degradation. Furthermore, most of these changes were similar to those observed in hypothalamic offspring astrocytes in culture. In conclusion, a maternal low caloric intake altered LM and ECS in both the hypothalamus and its astrocytes, pointing to these glial cells as responsible for a large part of the alterations seen in the total hypothalamus and suggesting a high degree of involvement of astrocytes in nutritional programming.

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The Lipolysome—A Highly Complex and Dynamic Protein Network Orchestrating Cytoplasmic Triacylglycerol Degradation

Metabolites ◽

10.3390/metabo10040147 ◽

2020 ◽

Vol 10 (4) ◽

pp. 147

Author(s):

Peter Hofer ◽

Ulrike Taschler ◽

Renate Schreiber ◽

Petra Kotzbeck ◽

Gabriele Schoiswohl

Keyword(s):

Lipid Metabolism ◽

Lysosomal Enzymes ◽

Cellular Localization ◽

Energy Homeostasis ◽

Hormone Sensitive Lipase ◽

Adipose Triglyceride Lipase ◽

Monoacylglycerol Lipase ◽

Sequential Action ◽

Binding Partners ◽

Hormone Sensitive

The catabolism of intracellular triacylglycerols (TAGs) involves the activity of cytoplasmic and lysosomal enzymes. Cytoplasmic TAG hydrolysis, commonly termed lipolysis, is catalyzed by the sequential action of three major hydrolases, namely adipose triglyceride lipase, hormone-sensitive lipase, and monoacylglycerol lipase. All three enzymes interact with numerous protein binding partners that modulate their activity, cellular localization, or stability. Deficiencies of these auxiliary proteins can lead to derangements in neutral lipid metabolism and energy homeostasis. In this review, we summarize the composition and the dynamics of the complex lipolytic machinery we like to call “lipolysome”.

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Purple bacteria as added-value protein ingredient in shrimp feed: Penaeus vannamei growth performance, and tolerance against Vibrio and ammonia stress

Aquaculture ◽

10.1016/j.aquaculture.2020.735788 ◽

2021 ◽

Vol 530 ◽

pp. 735788 ◽

Cited By ~ 2

Author(s):

Abbas Alloul ◽

Mathieu Wille ◽

Piergiorgio Lucenti ◽

Peter Bossier ◽

Gilbert Van Stappen ◽

...

Keyword(s):

Growth Performance ◽

Purple Bacteria ◽

Added Value ◽

Penaeus Vannamei ◽

Protein Ingredient ◽

Shrimp Feed ◽

Ammonia Stress

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Overexpression of Glucose-6-Phosphate Dehydrogenase Is Associated with Lipid Dysregulation and Insulin Resistance in Obesity

Molecular and Cellular Biology ◽

10.1128/mcb.25.12.5146-5157.2005 ◽

2005 ◽

Vol 25 (12) ◽

pp. 5146-5157 ◽

Cited By ~ 132

Author(s):

Jiyoung Park ◽

Ho Kyung Rho ◽

Kang Ho Kim ◽

Sung Sik Choe ◽

Yun Sok Lee ◽

...

Keyword(s):

Insulin Resistance ◽

Fatty Acids ◽

Lipid Metabolism ◽

Energy Homeostasis ◽

Marker Genes ◽

Necrosis Factor Alpha ◽

Diet Induced Obesity ◽

Insulin Dependent ◽

Glucose 6 Phosphate Dehydrogenase ◽

Interfering Rna

ABSTRACT Glucose-6-phosphate dehydrogenase (G6PD) produces cellular NADPH, which is required for the biosynthesis of fatty acids and cholesterol. Although G6PD is required for lipogenesis, it is poorly understood whether G6PD in adipocytes is involved in energy homeostasis, such as lipid and glucose metabolism. We report here that G6PD plays a role in adipogenesis and that its increase is tightly associated with the dysregulation of lipid metabolism and insulin resistance in obesity. We observed that the enzymatic activity and expression levels of G6PD were significantly elevated in white adipose tissues of obese models, including db/db, ob/ob, and diet-induced obesity mice. In 3T3-L1 cells, G6PD overexpression stimulated the expression of most adipocyte marker genes and elevated the levels of cellular free fatty acids, triglyceride, and FFA release. Consistently, G6PD knockdown via small interfering RNA attenuated adipocyte differentiation with less lipid droplet accumulation. Surprisingly, the expression of certain adipocytokines such as tumor necrosis factor alpha and resistin was increased, whereas that of adiponectin was decreased in G6PD overexpressed adipocytes. In accordance with these results, overexpression of G6PD impaired insulin signaling and suppressed insulin-dependent glucose uptake in adipocytes. Taken together, these data strongly suggest that aberrant increase of G6PD in obese and/or diabetic subjects would alter lipid metabolism and adipocytokine expression, thereby resulting in failure of lipid homeostasis and insulin resistance in adipocytes.

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Catalase deficiency facilitates the shuttling of free fatty acid to brown adipose tissue through lipolysis mediated by ROS during sustained fasting

10.21203/rs.3.rs-703630/v1 ◽

2021 ◽

Author(s):

Raghbendra Kumar Dutta ◽

Joon No Lee ◽

Yunash Maharjan ◽

Channy Park ◽

Seong-Kyu Choe ◽

...

Keyword(s):

Adipose Tissue ◽

Lipid Metabolism ◽

Brown Adipose Tissue ◽

Energy Homeostasis ◽

Redox Homeostasis ◽

Ros Generation ◽

Peroxisomal Enzyme ◽

Triglyceride Accumulation ◽

Brown Adipose

Abstract Background Fatty acids (FA) derived from adipose tissue and liver serve as the main fuel in thermogenesis of brown adipose tissue (BAT). Catalase, a peroxisomal enzyme, plays an important role in maintaining intracellular redox homeostasis by decomposing hydrogen peroxide to either water or oxygen that oxidize and provide fuel for cellular metabolism. Although the antioxidant enzymatic activity of catalase is well known, its role in the metabolism and maintenance of energy homeostasis has not yet been revealed. The present study investigated the role of catalase in lipid metabolism and thermogenesis during nutrient deprivation in catalase-knockout (KO) mice. Results We found that hepatic triglyceride accumulation in KO mice decreased during sustained fasting due to lipolysis through reactive oxygen species (ROS) generation in adipocytes. Furthermore, the free FA released from lipolysis were shuttled to BAT through the activation of CD36 and catabolized by lipoprotein lipase in KO mice during sustained fasting. Although the exact mechanism for the activation of the FA receptor enzyme is still unclear, we found that ROS generation in adipocytes mediated the shuttling of FA to BAT. Conclusions Taken together, our findings uncover the novel role of catalase in lipid metabolism and thermogenesis in BAT, which may be useful in understanding metabolic dysfunction.

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PPARs as Metabolic Regulators in the Liver: Lessons from Liver-Specific PPAR-Null Mice

International Journal of Molecular Sciences ◽

10.3390/ijms21062061 ◽

2020 ◽

Vol 21 (6) ◽

pp. 2061 ◽

Cited By ~ 13

Author(s):

Yaping Wang ◽

Takero Nakajima ◽

Frank J. Gonzalez ◽

Naoki Tanaka

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

Liver Cancer ◽

Energy Homeostasis ◽

Whole Body ◽

Lipid Homeostasis ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Metabolic Regulators

Peroxisome proliferator-activated receptor (PPAR) α, β/δ, and γ modulate lipid homeostasis. PPARα regulates lipid metabolism in the liver, the organ that largely controls whole-body nutrient/energy homeostasis, and its abnormalities may lead to hepatic steatosis, steatohepatitis, steatofibrosis, and liver cancer. PPARβ/δ promotes fatty acid β-oxidation largely in extrahepatic organs, and PPARγ stores triacylglycerol in adipocytes. Investigations using liver-specific PPAR-disrupted mice have revealed major but distinct contributions of the three PPARs in the liver. This review summarizes the findings of liver-specific PPAR-null mice and discusses the role of PPARs in the liver.

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Loss of Mrap2 is associated with Sim1 deficiency and increased circulating cholesterol

Journal of Endocrinology ◽

10.1530/joe-16-0057 ◽

2016 ◽

Vol 230 (1) ◽

pp. 13-26 ◽

Cited By ~ 23

Author(s):

T V Novoselova ◽

R Larder ◽

D Rimmington ◽

C Lelliott ◽

E H Wynn ◽

...

Keyword(s):

Lipid Metabolism ◽

Metabolic Regulation ◽

Energy Homeostasis ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Melanocortin Receptor ◽

Accessory Protein ◽

Loss Of Function ◽

Deficient Mice

Melanocortin receptor accessory protein 2 (MRAP2) is a transmembrane accessory protein predominantly expressed in the brain. Both global and brain-specific deletion of Mrap2 in mice results in severe obesity. Loss-of-function MRAP2 mutations have also been associated with obesity in humans. Although MRAP2 has been shown to interact with MC4R, a G protein-coupled receptor with an established role in energy homeostasis, appetite regulation and lipid metabolism, the mechanisms through which loss of MRAP2 causes obesity remains uncertain. In this study, we used two independently derived lines of Mrap2 deficient mice (Mrap2tm1a/tm1a) to further study the role of Mrap2 in the regulation of energy balance and peripheral lipid metabolism. Mrap2tm1a/tm1a mice have a significant increase in body weight, with increased fat and lean mass, but without detectable changes in food intake or energy expenditure. Transcriptomic analysis showed significantly decreased expression of Sim1, Trh, Oxt and Crh within the hypothalamic paraventricular nucleus of Mrap2tm1a/tm1a mice. Circulating levels of both high-density lipoprotein and low-density lipoprotein were significantly increased in Mrap2 deficient mice. Taken together, these data corroborate the role of MRAP2 in metabolic regulation and indicate that, at least in part, this may be due to defective central melanocortin signalling.

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