Fatty Acid Lipolysis Research Articles

Low Dietary Fish Meal Induced Endoplasmic Reticulum Stress and Impaired Phospholipids Metabolism in Juvenile Pacific White Shrimp, Litopenaeus vannamei.

This study mainly evaluated the low dietary fish-meal (FM) on growth performance, immune competence and metabolomics response of juvenile Pacific white shrimp, Litopenaeus vannamei reared at low salinity (7‰). Five experimental diets with graded levels (25, 20, 15, 10, and 5%) of FM were formulated. Weight gain, feed utilization and survival were decreased with the decreasing FM levels. When dietary FM decreased, glucose, cholesterol, total bile acids, and triglyceride in hemolymph decreased. Fatty acid synthesis was promoted and fatty acid lipolysis was reduced in hepatopancreas of shrimp fed low dietary FM. Endoplasmic reticulum (ER) stress related genes expression in hepatopancreas were down-regulated and in intestine were upregulated by low dietary FM. Inhibitor kappa B kinaseβ expression in intestine increased with the dietary FM levels, while mRNA levels of dorsal in hepatopancreas showed the opposite tendency. Hematoxylin and eosin (H&E) stain and transmission electron microscope analysis of intestinal samples indicated that low FM diets induced intestinal morphological damage, ER swollen and chromatin condensation. UPLC-Q/TOF-MS analysis indicated that degree of unsaturation of the fatty acid chains of phospholipids in hemolymph decreased with the decreasing dietary FM levels. Lysophospholipids and bile acids metabolism were disturbed by high levels of FM sparing in diet. These results indicated when dietary FM contents decreased, ER stress of shrimp was induced. The decreased unsaturated degree of phospholipids, decreased contents of lysophospholipids, altered lipid metabolism and ER stress may responsible for the impaired growth performance and health of shrimp fed a low FM diet.

An Alarm Pheromone May Be Released by Defeated Competitors: A Possible Indicator of Danger

Among many species, the establishment of hierarchical relations contains a highly ritualized behavioral context accompanied by the delivery of volatile agents, namely ketones and aldehydes, into environment. These substances act as signals contributing to defining and maintaining social hierarchies. Among mammals, some volatile compounds are released into the environment to report the presence of danger or conflict to conspecifics. For example, rats release an alarm pheromone, 2-heptanone, through their urine when subjected to physical stress. However, it is unknown whether some similarity occurs in human being, in spite that many possible alarm compounds have been identified in human fluids, including 2-heptanone. Contact sports may represent a situation of psychosocial interaction in which some hierarchy is established at the end of the contest. In such a case, the first match in martial arts competitions represents a natural model that is seemingly useful for studying alarm conditions in humans since there are two outcomes, winner and non-winner and after a stressful situation represented by contest, some kind of hierarchy is established. The present study measured urinary concentrations of 2-heptanone using gas chromatography-mass spectrometry and applied anxiety measures (State-Trait Anxiety Inventory, STAI) in a sample of healthy student athletes. Compared with martial-arts winners, the characteristics of the non-winners included an increase in their urinary 2-heptanone content (F2,18 = 5.541, p < 0.01), with no changes in anxiety scores (STAI-T: F2,18 = 0.052, p = 0.949; and STAI-S: F2,18 = 1.083, p = 0.360). The production of this ketone seems to be related with metabolic routes of fatty acids involving the participation of the so called stress hormones that may lead to an increase in the lipolysis of fatty acids and production of their metabolites, and among them, 2-heptanone. The increased release of 2-heptanone at the end of the match in non-winners may be interpreted as the release of an alarm signal that indicates imminent danger, similar to the occurrence in other species.

A decade of progress in adipose tissue macrophage biology.

One decade has passed since seminal publications described macrophage infiltration into adipose tissue (AT) as a key contributor to inflammation and obesity-related insulin resistance. Currently, a PubMed search for 'adipose tissue inflammation' reveals over 3500 entries since these original reports. We now know that resident macrophages in lean AT are alternatively activated, M2-like, and play a role in AT homeostasis. In contrast, the macrophages in obese AT are dramatically increased in number and are predominantly classically activated, M1-like, and promote inflammation and insulin resistance. Mediators of AT macrophage (ATM) phenotype include adipokines and fatty acids secreted from adipocytes as well as cytokines secreted from other immune cells in AT. There are several mechanisms that could explain the large increase in ATMs in obesity. These include recruitment-dependent mechanisms such as adipocyte death, chemokine release, and lipolysis of fatty acids. Newer evidence also points to recruitment-independent mechanisms such as impaired apoptosis, increased proliferation, and decreased egress. Although less is known about the homeostatic function of M2-like resident ATMs, recent evidence suggests roles in AT expansion, thermoregulation, antigen presentation, and iron homeostasis. The field of immunometabolism has come a long way in the past decade, and many exciting new discoveries are bound to be made in the coming years that will expand our understanding of how AT stands at the junction of immune and metabolic co-regulation.