LITERATURE SURVEY - GLUCONEOGENESIS AND A MINO-ACIDS IN RUMINANTS

Gluconeogenesis (GN) is of prime importance in ruminant as only small amounts of glucose reach the duodenum to be absorbed. One of the limit ing factors of GN is substrate availability: unlike nonruminants in wh ich the rate of GN is higher during fasting, in ruminants, it is maxim al after feeding, as a result of the availability of propionate from t he fermented dietary carbohydrates in the rumen. However, certain meta bolites present in portal blood such as ammonia, butyrate and especial ly ethanol, may inhibit the conversion of propionate into glucose. In contrast to its action on propionate, ethanol would stimulate GN from amino acids through an increase of cortisol secretion and an elevation of intracellular cAMP and calcium levels. In order to ensure glycemia homeostasis, glucose metabolism in hepatic tissue of ruminants is ada pted to the specificities of carbohydrate digestion in the rumen. The lack of portal increase in glycemia during the postprandial period and the necessity of a metabolic GN-propionate dependent activity during that period, is compensated by a low activity of both liver hexokinase and glucokinase which, in simple-stomached animals, act to maintain g lucose in the liver. Moreover, phosphoenolpyruvate carboxykinase (PEPC K) which is highly adaptive to gluconeogenic needs in nonruminants, sh ows little adaptation in ruminants during starvation. During energetic underfeeding and starvation periods, propionate contribution to gluco se synthesis decreases markedly whereas that of amino acids, glycerol and lactate increases. This is accompanied by fat mobilization from ad ipose tissues and ketone bodies synthesis from the liver to partly mee t the energetic needs. In both ruminant and nonruminant, the main gluc ogenic amino acids are primarily alanine and glutamine. Blood levels o f certain hormones (insulin, glucagon, growth hormone, glucocorticoids , catecholamines) can fluctuate according to the physiological (pregna ncy, lactation, growth) and the nutritional status of the animals, whi ch in turn have an influence on the intensity of hepatic and accessory renal GN.