Search Results

You are looking at 51 - 60 of 1,135 items for :

  • "metabolism" x
Clear All
Free access

Verónica Sancho, María V Trigo, Nieves González, Isabel Valverde, Willy J Malaisse and María L Villanueva-Peñacarrillo

-like stimulatory effects upon glucose transport and metabolism in normal ( Valverde et al. 1994 , Villanueva-Peñacarrillo et al. 1994 , Luque et al. 2002 ) and diabetic ( Morales et al. 1997 , López-Delgado et al. 1998 ) states; in addition, this

Free access

R Mindnich, F Haller, F Halbach, G Moeller, M Hrabé de Angelis and J Adamski

been studied in detail and in both species the enzyme does not seem to be involved in androgen metabolism. To get more insight into the molecular regulation of androgen function in fish, we identified and analyzed 17β-HSD type 3 in zebrafish with

Restricted access

L. Desrues, M. C. Tonon and H. Vaudry


Previous studies have demonstrated that TRH is a potent stimulator of α-MSH secretion from frog pituitary melanotrophs. In order to determine the intracellular events responsible for TRH-evoked α-MSH release, we have investigated the effect of TRH on polyphosphoinositide breakdown in frog pars intermedia. Neurointermediate lobes were labelled to isotopic equilibrium with myo-[3H]inositol.

TRH stimulated the rate of incorporation of [3H]inositol into the phospholipid fraction. The effect of TRH was concentration-dependent; half-maximal stimulation of α-MSH release and inositol incorporation occurred at 12 and 28 nmol TRH/1 respectively. In prelabelled neurointermediate lobes, lithium (10 mmol/l) enhanced the radioactivity in inositol monophosphate, bisphosphate (IP2) and trisphosphate (IP3). LiCl (10 mmol/l) induced a 38% inhibition of α-MSH release from perifused neurointermediate lobes but did not impair TRH-induced α-MSH secretion. In the presence of LiCl, TRH (1 μmol/l) induced a transient increase of the radioactivity in IP3, which was evident by 30 s and maximal by 1 min (+ 100%). TRH treatment also increased the radioactivity in IP2, which reached a plateau after 5 min (+ 100%). The increase in radioactivity in IP3 induced by TRH was closely paralleled by a rapid loss of [3H]phosphatidylinositol bisphosphate (PIP2), which was maximal by 1 min (−70%).

These results indicate that, in frog pars intermedia, TRH-evoked α-MSH secretion is coupled to breakdown of PIP2. The data suggest that, in amphibian melanotrophs, as previously shown in GH3 tumour cells and in rat pituitary mammotrophs, TRH causes rapid stimulation of polyphosphoinositide-hydrolysing phospholipase C.

Restricted access

Bolander FF Jr, E Ginsburg and BK Vonderhaar

In a previous study, infection with the mouse mammary tumor virus (MMTV) was shown to increase the sensitivity of the mammary epithelium toward prolactin (PRL); furthermore, this effect could be mimicked by the binding of the MMTV envelope protein (gp52) to its cell receptor. The present work has investigated the possibility that gp52-induced changes in the PRL receptor (PRLR) were responsible for this phenomenon. In vitro, gp52 doubled the PRLR concentration in the plasmalemma of mammary epithelium without affecting the affinity. The origins of these PRLRs were twofold: first, gp52 stimulated PRLR mRNA nearly fivefold, suggesting that some of the receptors were newly synthesized. Second, there was a redistribution of PRLRs within the mammary cell: PRLRs were shifted from an internal pool to the plasma membrane. This relocation was very rapid, occurring within 30 min. There did not appear to be any contribution from alterations in PRLR degradation, since the half-life of PRLR was not affected by gp52. In summary, the MMTV increases the PRL sensitivity of mouse mammary epithelium by elevating PRLRs through both enhanced synthesis and recruitment from microsomes.

Free access

FM Ng, WJ Jiang, R Gianello, S Pitt and P Roupas

A lipolytic domain (AOD9401) of human growth hormone (hGH) which resides in the carboxyl terminus of the molecule and contains the amino acid residues 177-191, has been synthesized using solid-phase peptide synthesis techniques. AOD9401 stimulated hormone-sensitive lipase and inhibited acetyl coenzyme A carboxylase (acetyl CoA carboxylase) in isolated rat adipose tissues, in a similar manner to the actions of the intact hGH molecule. The synthetic lipolytic domain mimicked the effect of the intact growth hormone on diacylglycerol release in adipocytes. Chronic treatment of obese Zucker rats with AOD9401 for 20 days reduced the body weight gain of the animals, and the average cell size of the adipocytes of the treated animals decreased from 110 to 80 microm in diameter. Unlike hGH, synthetic AOD9401 did not induce insulin resistance or glucose intolerance in the laboratory animals after chronic treatment. The results suggest that AOD9401 has the potential to be developed into a therapeutic agent for the control of obesity.

Free access

Suryaprakash Raichur, Song Hooi Teh, Kenji Ohwaki, Vidhi Gaur, Yun Chau Long, Mark Hargreaves, Sean L McGee and Jun Kusunoki

energy gauge, which is activated by alterations in the cellular AMP to ATP ratio and by hormones that signal low energy status ( Kahn et al . 2005 ). In skeletal muscle, AMPK is thought to control metabolism not only by acute regulation of metabolic

Free access

Xilin Yang, Zezhang Tao, Zhanyong Zhu, Hua Liao, Yueqiang Zhao and Huajun Fan

central role in the metabolism of fats and carbohydrates ( Thirone et al . 2006 , Liao et al . 2010 ). When control of insulin levels fails, glucose metabolism disorders can result and can culminate in diabetes. Disturbances of glucose metabolism are

Free access

Emily Tubbs and Jennifer Rieusset

Introduction Cellular metabolism is closely regulated and compartmentalized within distinct subcellular organelles. Mitochondria and endoplasmic reticulum (ER) play a crucial role in these processes, as their structure and function are

Free access

Janne Lebeck

Glycerol metabolism The metabolic switching between feeding and fasting is central to everyday life and involves tight hormonal control with effects on muscle, adipose tissue, and liver that maintains an adequate handling of metabolic precursors to

Free access

Suzy S J Hur, Jennifer E Cropley and Catherine M Suter

daughters ( Fontelles et al . 2016 ). The catalog of paternally programmed phenotypes is fast growing, and the most numerous examples are those that involve programming of offspring metabolism. The purpose of this review is to outline the evidence for