The gill microbiota of invasive and indigenous Spondylus oysters from the Mediterranean Sea and northern Red Sea.

The gill tissue of bivalve mollusks hosts rich symbiotic microbial communities that may contribute to the animal's metabolism. Spondylus spinosus is an invasive oyster that has become highly abundant along the eastern Mediterranean Sea (EMS) coastline, but is scarce in the northern Red Sea (NRS), its indigenous region. The composition and seasonal dynamics of the gill microbial communities of S.

Phosphoenolpyruvate carboxykinase (Pck1) helps regulate the triglyceride/fatty acid cycle and development of insulin resistance in mice.

The aim of this study was to investigate the role of the cytosolic form of phosphoenolpyruvate carboxykinase (Pck1) in the development of insulin resistance. Previous studies have shown that the roles of Pck1 in white adipose tissue (WAT) in glyceroneogenesis and reesterification of free fatty acids (FFA) to generate triglyceride are vital for the prevention of diabetes. We hypothesized that insulin resistance develops when dysregulation of Pck1 occurs in the triglyceride/fatty acid cycle, which regulates lipid synthesis and transport between adipose tissue and the liver.

Glyceroneogenesis, the pathway that almost wasn't.

"What seest thou else in the dark, backward abysm of time." Prospero in The Tempest As is true in all aspects of human endeavor, a scientific concept can appear before its time and remain unappreciated before events catch up with the concept. Such was the case of the discovery of glyceroneogenesis and the establishment of its biological importance; it took almost 40 years before the significance of this pathway became apparent and the concept of triglyceride recycling was understood by the scientific establishment.

Phosphoenolpyruvate carboxykinase and the critical role of cataplerosis in the control of hepatic metabolism.

Background: The metabolic function of PEPCK-C is not fully understood; deletion of the gene for the enzyme in mice provides an opportunity to fully assess its function.

Methods: The gene for the cytosolic form of phosphoenolpyruvate carboxykinase (GTP) (EC 4.1.

Glucocorticoids regulate transcription of the gene for phosphoenolpyruvate carboxykinase in the liver via an extended glucocorticoid regulatory unit.

The hepatic transcriptional regulation by glucocorticoids of the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK-C) gene is coordinated by interactions of specific transcription factors at the glucocorticoid regulatory unit (GRU). We propose an extended GRU that consists of four accessory sites, two proximal AF1 and AF2 sites and their distal counterpart dAF1 (-993) and a new site, dAF2 (-1365); together, these four sites form a palindrome. Sequencing and gel shift binding assays of hepatic nuclear proteins interacting with these sites indicated similarity of dAF1 and dAF2 sites to the GRU proximal AF1 and AF2 sites.

Factors that control the tissue-specific transcription of the gene for phosphoenolpyruvate carboxykinase-C.

Transcription of the gene for PEPCK-C occurs in a number of mammalian tissues, with highest expression occurring in the liver, kidney cortex, and white and brown adipose tissue. Several hormones and other factors, including glucagon, epinephrine, insulin, glucocorticoids and metabolic acidosis, control this process in three responsive tissues, liver, adipose tissue, and kidney cortex. Expression of the gene in these three tissues in regulated in a different manner, responding to the specific physiological role of the tissue.

Glyceroneogenesis revisited.

Glyceroneogenesis is the synthesis of 3-glycerol phosphate by an abbreviated version of gluconeogenesis. The research that led to the discovery of glyceroneogenesis in white adipose tissue is presented. This pathway is active during fasting in white and brown adipose tissue and in the liver as part of the triglyceride/fatty acid cycle.

The transcriptional regulation of phosphoenolpyruvate carboxykinase gene in the kidney requires the HNF-1 binding site of the gene.

The transcription of the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK-C) gene is differentially regulated in each of the several PEPCK-C-expressing tissues. In the kidney, it is regulated by glucocorticoids and acidosis. Previously, we reported that in LLC-PK1 and derived kidney cell lines, mutation of the hepatic nuclear factor 1 (HNF-1) binding site in PEPCK-C gene promoter markedly reduced both the basal activity of the gene promoter and its response to acidic pH.

Glucocorticoids repress transcription of phosphoenolpyruvate carboxykinase (GTP) gene in adipocytes by inhibiting its C/EBP-mediated activation.

The cytosolic form of the phosphoenolpyruvate carboxykinase (PEPCK-C) gene is selectively expressed in several tissues, primarily in the liver, kidney, and adipose tissue. The transcription of the gene is reciprocally regulated by glucocorticoids in these tissues. It is induced in the liver and kidney but repressed in the white adipose tissue.

A mutation in the peroxisome proliferator-activated receptor gamma-binding site in the gene for the cytosolic form of phosphoenolpyruvate carboxykinase reduces adipose tissue size and fat content in mice.

Regulation of the turnover of triglycerides in adipose tissue requires the continuous provision of 3-glycerophosphate, which may be supplied by the metabolism of glucose or by glyceroneogenesis, the de novo synthesis of 3-glycerophosphate from sources other than hexoses or glycerol. The importance of glyceroneogenesis in adipose tissue was assessed in mice by specifically eliminating the expression of the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK-C), an enzyme that plays a pivotal role in the pathway. To accomplish this, we mutated the binding site for the peroxisome proliferator-activated receptor gamma (PPAR gamma) called the peroxisome proliferator-activated receptor element (PPARE), in the 5' flanking region of the PEPCK-C gene in the mouse by homologous recombination.