China
Africa
Explore chapters and articles related to this topic
Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
In this chapter, we present a contemporary view of molecular sport nutrition by providing the molecular exercise physiologist or sport nutritionist with an understanding of the molecular processes supporting fundamental principles of performance nutrition. After a brief introduction of how appetite is controlled, we proceed to discuss the molecular pathways that control muscle glucose uptake and glycogen storage. Such processes support the fundamental principle of carbohydrate (CHO) loading (i.e. the supercompensation of muscle glycogen stores prior to intense and prolonged exercise). In keeping with the theme of “fuels for the fire”, we then outline the molecular pathways supporting “fat adaptation” protocols, a nutritional strategy that can be employed to enhance IMTG storage and spare the use of muscle glycogen during exercise. Having considered the basis of energy storage, we subsequently provide a critical overview of how the availability of nutrients supports muscle protein synthesis (MPS) and oxidative adaptations in human skeletal muscle. In relation to the latter, specific attention is given to the role of reduced CHO availability in regulating mitochondrial biogenesis, the so-called “train-low” strategy. Due to space constraints, it is not possible to build upon themes presented in the previous edition of this chapter. For a detailed discussion on principles of nutrient sensing by target tissues such as the brain and muscle, the reader is therefore directed to the previous edition of this textbook, and chapter by Hamilton et al. (2014).
Placental transport and metabolism
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
A relatively recent addition to the armamentarium regulating placental transport activity (maternal nutritional status, placental blood flow, maternal/placental hormone production, hypoxia) is mammalian target of rapamycin (mTOR). A serine/threonine kinase, mTOR protein is expressed in the cytosol of the syncytiotrophoblast and is thought to regulate cell growth by its influence on translation and transcription through a mechanism of “nutrient sensing” (33). This refers to a proposed process whereby mTOR regulates production of proteins related to cell growth in response to the placental environment, including nutrient availability, oxygenation, and growth factors. These proteins regulate nutrient transporters and thereby affect fetal growth. In vitro data supporting the proposed role of mTOR in fetal growth include the finding that the activity of the mTOR signaling pathway is down-regulated in IUGR and that inhibition of mTOR resulted in nearly complete inhibition of leucine uptake by the system L amino acid transporter (34).
Energy Metabolism, Metabolic Sensors, and Nutritional Interventions in Polycystic Kidney Disease
Published in Jinghua Hu, Yong Yu, Polycystic Kidney Disease, 2019
Sonu Kashyap, Eduardo Nunes Chini
In eukaryotes, metabolism is tightly controlled by nutrient and energy sensing pathways involving several metabolic sensors such as the mammalian target of rapamycin (mTOR) pathways, AMP-activated protein kinase (AMPK), and sirtuins (Figure 8.1). These metabolic sensors monitor nutrient availability and control metabolic adaptations in cells in response to environmental changes.8 Interestingly, several studies indicate that these metabolic sensors also play a key role in the pathogenesis of ADPKD.9–11 mTOR is the central regulator of the nutrient-sensing signaling pathway that controls cellular metabolism, protein synthesis, and cell growth. In fact, the first evidence recognizing the role of metabolism in ADPKD was the finding that mTOR plays a key role in the pathogenesis of this disease.12 Elevated mTOR activity has been reported in ADPKD and is considered a major driver of cell proliferation.11 Moreover, the inhibition of this pathway with rapamycin and other rapalogs is protective in experimental PKD.11,13,14 The mTOR pathway is negatively regulated by the metabolic sensor AMPK, and activation of AMPK also reduces the cystogenesis in ADPKD.9 Activation of SIRT1, a nicotinamide adenine dinucleotide-dependent (NAD-dependent) deacetylase also plays a role in the pathogenesis of ADPKD, and its inhibition shows a delay in cyst formation and growth.10,15 These findings indicated that metabolic alterations play a key role in the pathogenesis of ADPKD.
Percentages of serum, liver and adipose tissue fatty acids and body weight are affected in female rats by long-term Central kisspeptin treatments
Published in Archives of Physiology and Biochemistry, 2023
Zafer Sahin, Mete Ozcan, Ahmet Ozkaya, Sinan Canpolat, Selim Kutlu, Haluk Kelestimur
In recent years, there have been important reports that the Kiss1r knockout mouse exhibits metabolic dysfunction and suggests a key role for kisspeptin signalling in regulating the metabolism (Tolson et al. 2014, 2016). However, it has been suggested that adipocyte differentiation and fat accumulation occur in Kiss1r−/− mice, and therefore, the kisspeptin receptor may has a role in the pathogenesis of direct obesity (Wang et al.2018). Fatty acids (FAs) and lipids are an important source of energy. Fatty acids have been shown to play many important roles in biological processes, either directly or through their modifications. Most of the processes involved in the FA metabolism have been now shown to be controlled by hormones and neuropeptides (Bhathena 2006). Nutrient sensing within the hypothalamus has a critical role in the complex network of signals controlling the energy metabolism (Cota et al. 2007, Le Foll et al. 2009, Moran 2010). In addition to hormonal signals, nutrients crossing the blood–brain barrier, such as glucose and lipids, affect central control of food intake and energy expenditure (Cota et al. 2007, Le Foll et al. 2009). Fatty acids also alter hormone receptors by altering lipid milieu and the composition and fluidity of cell membranes. Additionally, many metabolic processes altered by FAs or their metabolites, such as platelet aggregation, activities of many enzymes and metabolic disorders such as diabetes, atherosclerosis and hypertension, have a strong endocrine component (Bhathena 2006).
Cinnamaldehyde attenuates kidney senescence and injury through PI3K/Akt pathway-mediated autophagy via downregulating miR-155
Published in Renal Failure, 2022
Weakened kidney function with advancing age is probably attributed to multiple factors [1], among which autophagy is reported to play a fundamental role [9]. Autophagy is a multistep and dynamic process, during which highly regulated lysosomal proteins are degraded to recycle damaged or excess organelles and protein aggregates for maintaining intracellular homeostasis and cellular innovation [10]. Moreover, metabolic slowdown is a common feature of cell aging, bringing about negative situations that toxic wastes in the body fail to be excreted in a timely manner. As a result, toxic wastes can accumulate and cause long-term damage to tissues, cells, and protein functions, thereby reducing the survival rate of cells and affecting the lifespan of the body [11,12]. Autophagy works excellent in decomposing damaged proteins and cells, and using them repeatedly to extend the life of cells and delay the body’s aging, showing its potential in regulating cell senescence [12,13]. A previous study has shown that inhibition of autophagy in the kidney is associated with the aging-caused degeneration of proximal tubular cells [14]. Furthermore, several major nutrient-sensing pathways such as adenosine monophosphate-activated protein kinase (AMPK), sirtuin 1 and mammalian target of rapamycin (mTOR) are inferred to play regulatory roles in autophagy during kidney senescence [15–17].
Can we make drug discovery targeting fundamental mechanisms of aging a reality?
Published in Expert Opinion on Drug Discovery, 2022
David G. Le Couteur, Rozalyn M. Anderson, Rafael de Cabo
Another strategy is repurposing, where new indications are found for drugs that have been studied and/or registered for other indications. For aging drugs, this was successful for calorie restriction-mimetics. Calorie restriction delays aging via pathways that include the nutrient sensing proteins: mechanistic target of rapamycin (MTOR) and AMP-activated protein kinase (AMPK). The immunosuppressant drug, rapamycin, inhibits MTOR and the antidiabetic drug, metformin is thought to activate AMPK, although both drugs have other effects that could influence aging. These drugs increase lifespan in animals and recapitulate some, but not all, of the biologic effects of caloric restriction. At the molecular level, such as gene expression, there are significant differences, and neither metformin or rapamycin could be considered to be caloric restriction mimetics [12]. Metformin and rapamycin both have established safety profiles as treatment for other indications, therefore, it has been proposed that these two drugs should be the first to be evaluated in long term trials as aging therapies in humans [13]. In general, the costs of repurposing known drugs for aging will still be substantial and will require comprehensive aging studies in animals.