Glucose entry into cells

Insulin stimulates fatty acid synthesis by stimulating glucose entry into cells and activating pyruvate dehydrogenase complex. 

Glucose entry into most cells is concentration driven and independent of sodium. Four glucose transporters (GLUT) are listed in Table 1-12-1. They have different afiinities for glucose coinciding with their respective physiologic roles. Normal glucose concentration in peripheral blood is 4-8 mM (70-140 m dL). 

Parenteral /32-agonists such as albuterol (salbuta-mol) increase the activity of the membrane sodium-potassium ATPase, and so increase potassium entry into cells. Nebulized or infused albuterol (salbutamol) significantly lowers serum potassium concentration over 5 hours. A suitable initial dose of nebulized albuterol is 5 mg in adults. It can provoke tremor and tachyarrhythmia, and it is desirable to monitor cardiac rhythm during nebulization. The combination of nebulized albuterol (salbutamol) with infusion of insulin + glucose is more effective than the infusion alone. 

Diagrammatic representation of insulin secretion from pancreatic fi cells. The sequence of events of insulin secretion coupled to glucose entry into fi cells consists of glucokinase action, ATP production, inhibition of the ATP-sensitive K+ channel, membrane depolarization, Ca + influx, and insulin release. Neurotransmitters acetylcholine and norepinephrine stimulate and inhibit insulin secretion via trimeric G-proteins Gq and Gj, respectively. Glucagon-like peptide (GLP) promotes insulin release via the G-protein G. Sulfonamides and diazoxide have direct effects on sulfonylurea receptors (SURs) the former promotes insulin release and the latter inhibits insulin release. +, Stimulation —, inhibition. Other abbreviations are given in the text. 

Glucose and insulin treatment, which increases the rate of potassium entry into cells. 

Insulin is secreted by the pancreatic P-cells and is required for the S5mthesis of the glucose storage polymer glycogen and is also required for the entry of glucose into tissues. Reduced glucose entry into tissues is the major effect of insulin deficiency and this produces an increased level of... 

The entry of CL into cells may be essential for the cellular entry [232] or secretion [233] of some macromolecules such as diphtheria toxin and modeccin. Sandvig and Olsnes [232] studied the entry of diphtheria toxin and modeccin into Vero cells in pH 7.2 media containing 20 mM Hepes, 1 mM Ca(OH)2, 5 mM glucose,a sufficient amount of mannitol to ensure isotonicity, and varying concentrations of NaCl. The cellular uptake of 0.1 nM diphtheria toxin at the end of 50 min was strongly dependent on CL concentration. It was 0% at 0 mM NaCl, 25% of the 140 mM NaCl control at 2 mM NaCl, and 60% of the control at 70 mM NaCl. A similar trend was observed for modeccin, i.e., no transport at 0 mM NaCl, 20% of control at 0.05 mM NaCl, 60% of control at 0.1 mM NaCl, 80% of control at 0.5 mM NaCl, and 100% of control at 2 mM NaCl. 

About ten percent of the calories contained in the Western diet are supplied by fructose (approximately fifty g/day). The major source of fructose is the disaccharide sucrose, which, when cleaved in the intestine, releases equimolar amounts of fructose and glucose (see p. 86). Fructose is also found as a free monosaccharide in high-fructose corn syrup (55 percent fructose/45 percent glucose, which is used to sweeten most cola drinks), in many fruits, and in honey. Entry of fructose into cells is not insulin-dependent (unlike that of glucose into certain tissues, see p. 95), and, in contrast to glucose, fructose does not promote the secretion of insulin. 

Major source of fructose The major source of fructose is sucrose, which, when cleaved, releases equimolar amounts of fructose and glucose. Entry of fructose into cells is insulin-independent. 

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