Feeding versus fasting

Feeding versus fasting. Mona A Hussain Assistant Prof. In medical Physiology department FOM - PSU.

The absorptive state. 1-The absorptive ( well-fed ) state is the 2- to 4-hour period after ingestion of a normal meal . 2- During this interval , transient increase s in plasma glucose , amino acids , and triacylglycerols (TAG) occur. 3- Islet tissue of the pancreas responds to the elevated levels of glucose with an increased secretion of insulin and a decreased release of glucagon . The elevated insulin-to-glucagon ratio and the ready availability of circulating substrates make the absorptive state an anabolic period characterized by increased synthesis of TAG and glycogen to replenish fuel stores and enhanced synthesis of protein . 4- During this absorptive period , virtually all tissues use glucose as a fuel 5- The metabolic response of the body is dominated by alterations in the metabolism of liver , adipose tissue , skeletal muscle , and brain ..

Fasting (Post absorptive state). Fasting begins if no food is ingested after the absorptive period . It may result from an inability to obtain food, the desire to lose weight rapidly , or clinical situations in which an individual cannot eat ( for example , because of trauma , surgery , cancer , or burns ). In the absence of food, plasma levels of glucose, amino acids, and TAG fall, triggering a decline in insulin secretion and an increase in glucagon and epinephrine release . The decreased insulin/counter regulatory hormone ratio and the decreased availability of circulating substrates make the period of nutrient deprivation a catabolic period characterize d by de gradation of TAG, glycogen , and protein . Has two priorities: 1 ) the need to maintain adequate plasma levels of glucose to sustain energy metabolism in the brain, red blood cells , and other glucose-requiring tissues 2 ) the need to mobilize fatty acids from adipose tissue and the synthesis and release of ketone bodies from the liver to supply energy to other tissues..

Fuel stores (in 70 Kg man at the beginning of a fast).

Liver in Well-fed period VS Fasting (Carbohydrate metabolism).

Liver in Well-fed period VS Fasting (Fat metabolism).

Liver in Well-fed period VS Fasting (Protein metabolism).

ADIPOSE TISSUE : ENERGY STORAGE DEPOT (Carbohydrate metabolism).

ADIPOSE TISSUE (Fat metabolism). Well-Feeding Most of the FAs added to the TAG stores of adipocytes after consumption of a lipid-containing meal are provided by the degradation of exogenous (dietary) TAG sent out by the intestine and endogenous TAG in VLDL sent out by the liver..

Resting skeletal muscle (carbohydrate). Well-Feeding increase in glucose transport into muscle cells by GLUT-4 Increased glycogen synthesis.

Resting skeletal muscle (Protein). Well-Feeding Increased protein synthesis Increased uptake of branched-chain amino acids.

Resting skeletal muscle (fat metabolism). Well-Feeding fatty acids are of secondary importance as a fuel for resting muscle during the fed state , in which glucose is the primary source of energy ..

Brain. The brain exclusively use s glucose a s a fuel (GLUT-1 of the BBB is insulin independent ), completely oxidizing approximately 140 g/day to CO2 and H2O . The brain contains no significant store s of glycogen and is , therefore , completely dependent on the availability of blood glucose. If blood glucose levels fall below 40 mg/100 ml, cerebral function is impaired The brain also lacks significant stores of TAG, and the FAs circulating in the blood make little contribution to energy production be cause FAs bound to albumin do not efficiently cross the BBB.

Kidney and long term fasting. Gluconeogenesis (50% come from the kidneys) Compensation for ketoacidosis Glutaminase and ammonia.

Role of insulin. Action of Insulin Increases glucose uptake into cells Increases glycogen formation Decreases glycogenolysis Decreases gluconeogenesis Increases protein synthesis (anabolic) Increases fat deposition Decreases lipolysis Increases K* uptake into cells Effect on Blood Level Decreases blood [glucose] Decreases blood [amino acid] Decreases blood [fatty acid] Decreases blood [ketoacid] Decreases blood [K*].

Role of Glucagon. Action of Glucagon Increases glycogenolysis Increases gluconeogenesis Increases lipolysis Increases ketoacid formation Effect on Blood Level Increases blood [glucose] Increases blood [fatty acid] Increases blood [ketoacid].

TABLE 16.3 Effects of CortüA Organk L Basal concentrations are permissive for stimulation of gluccyrc*errsis arid liFx)lysis in tir pcstBorvRive II. Increard plasma conæntrations A. incre.aæd prckein B. incre.aæd gluconeoprsis. C. &creaæd uptake by muscle cells and adipose-tisszr ælls. D. break&ywn- Increaæd plasma concentratk»ns of amino acids, glucoæ, and free fatty acids.

TABLE 16.4 Glycoplysis Glucorogeresis Liplysis Sunmary of Ghme.Counterrgulatory F*phrim Cortid Growth Ibrnm Inhibition of glucoe uptake by muscle cells and adipe tissu: cells 'A / press; illiaeslhu hu m mw m Li prom Epi*ite in Ijer *reu a Ijet.

Abs o • NO e or •e a to to or boa... Of any 24.20 E' s t cycle VLDL ve icy.