↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg. 502.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg. 503.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., p. 23.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 544.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 568.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 633.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 640.
↑ Masood W, Annamaraju P, Khan Suheb MZ, et al. Ketogenic Diet. [Updated 2023 Jun 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499830/
↑ Devrim-Lanpir, Aslı, Lee Hill, and Beat Knechtle. 2021. "Efficacy of Popular Diets Applied by Endurance Athletes on Sports Performance: Beneficial or Detrimental? A Narrative Review" Nutrients 13, no. 2: 491. https://doi.org/10.3390/nu13020491
1 2 Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 731.
↑ Nelson, David L., Cox, Michael M. Lehninger: Principles of Biochemistry. New York: W.H. Freeman and Company, 2013. Sixth ed., pg 734.
↑ Robert K. Crane, D. Miller and I. Bihler. "The restrictions on possible mechanisms of intestinal transport of sugars". In: Membrane Transport and Metabolism. Proceedings of a Symposium held in Prague, August 22–27, 1960. Edited by A. Kleinzeller and A. Kotyk. Czech Academy of Sciences, Prague, 1961, pp. 439-449.
↑ Wright, Ernest M.; Turk, Eric (2004). "The sodium glucose cotransport family SLC5". Pflügers Arch. 447 (5): 510–8. doi:10.1007/s00424-003-1063-6. PMID12748858. Crane in 1961 was the first to formulate the cotransport concept to explain active transport [7]. Specifically, he proposed that the accumulation of glucose in the intestinal epithelium across the brush border membrane was coupled to downhill Na+ transport cross the brush border. This hypothesis was rapidly tested, refined and extended [to] encompass the active transport of a diverse range of molecules and ions into virtually every cell type.
↑ Boyd, C A R (2008). "Facts, fantasies and fun in epithelial physiology". Experimental Physiology. 93 (3): 303–14. doi:10.1113/expphysiol.2007.037523. PMID18192340. the insight from this time that remains in all current text books is the notion of Robert Crane published originally as an appendix to a symposium paper published in 1960 (Crane et al. 1960). The key point here was 'flux coupling', the cotransport of sodium and glucose in the apical membrane of the small intestinal epithelial cell. Half a century later this idea has turned into one of the most studied of all transporter proteins (SGLT1), the sodium–glucose cotransporter.
↑ Malenka RC, Nestler EJ, Hyman SE (2009). Sydor A, Brown RY (penyunting). Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ed. 2nd). New York: McGraw-Hill Medical. m/s. 179, 262–263. ISBN9780071481274. Orexin neurons are regulated by peripheral mediators that carry information about energy balance, including glucose, leptin, and ghrelin. ... Accordingly, orexin plays a role in the regulation of energy homeostasis, reward, and perhaps more generally in emotion. ... The regulation of energy balance involves the exquisite coordination of food intake and energy expenditure. Experiments in the 1940s and 1950s showed that lesions of the lateral hypothalamus (LH) reduced food intake; hence, the normal role of this brain area is to stimulate feeding and decrease energy utilization. In contrast, lesions of the medial hypothalamus, especially the ventromedial nucleus (VMH) but also the PVN and dorsomedial hypothalamic nucleus (DMH), increased food intake; hence, the normal role of these regions is to suppress feeding and increase energy utilization. Yet discovery of the complex networks of neuropeptides and other neurotransmitters acting within the hypothalamus and other brain regions to regulate food intake and energy expenditure began in earnest in 1994 with the cloning of the leptin (ob, for obesity) gene. Indeed, there is now explosive interest in basic feeding mechanisms given the epidemic proportions of obesity in our society, and the increased toll of the eating disorders, anorexia nervosa and bulimia. Unfortunately, despite dramatic advances in the basic neurobiology of feeding, our understanding of the etiology of these conditions and our ability to intervene clinically remain limited.
↑ "Neurobiology of food intake in health and disease". Nat. Rev. Neurosci. 15 (6): 367–378. 2014. doi:10.1038/nrn3745. PMC4076116. PMID24840801. However, in normal individuals, body weight and body fat content are typically quite stable over time2,3 owing to a biological process termed ‘energy homeostasis’ that matches energy intake to expenditure over long periods of time. The energy homeostasis system comprises neurons in the mediobasal hypothalamus and other brain areas4 that are a part of a neurocircuit that regulates food intake in response to input from humoral signals that circulate at concentrations proportionate to body fat content4-6. ... An emerging concept in the neurobiology of food intake is that neurocircuits exist that are normally inhibited, but when activated in response to emergent or stressful stimuli they can override the homeostatic control of energy balance. Understanding how these circuits interact with the energy homeostasis system is fundamental to understanding the control of food intake and may bear on the pathogenesis of disorders at both ends of the body weight spectrum.
