The problem of nitrogen disposal in the obese

Abstract

Amino-N is preserved because of the scarcity and nutritional importance of protein. Excretion requires its conversion to ammonia, later incorporated into urea. Under conditions of excess dietary energy, the body cannot easily dispose of the excess amino-N against the evolutively adapted schemes that prevent its wastage; thus ammonia and glutamine formation (and urea excretion) are decreased. High lipid (and energy) availability limits the utilisation of glucose, and high glucose spares the production of ammonium from amino acids, limiting the synthesis of glutamine and its utilisation by the intestine and kidney. The amino acid composition of the diet affects the production of ammonium depending on its composition and the individual amino acid catabolic pathways. Surplus amino acids enhance protein synthesis and growth, and the synthesis of non-protein-N-containing compounds. But these outlets are not enough; consequently, less-conventional mechanisms are activated, such as increased synthesis of NO z followed by higher nitrite (and nitrate) excretion and changes in the microbiota. There is also a significant production of N 2 gas, through unknown mechanisms. Health consequences of amino-N surplus are difficult to fathom because of the sparse data available, but it can be speculated that the effects may be negative, largely because the fundamental N homeostasis is stretched out of normalcy, forcing the N removal through pathways unprepared for that task. The unreliable results of hyperproteic diets, and part of the dysregulation found in the metabolic syndrome may be an unwanted consequence of this N disposal conflict.

Altered Nitrogen Balance and Decreased Urea Excretion in Male Rats Fed Cafeteria Diet Are Related to Arginine Availability

“…It has been postulated that a high-energy diet coupled with normal or increased protein intake may hamper 2-amino nitrogen elimination in rats, humans, and other mammals [33]. This problem is largely a consequence of the abundance of energy, mainly in the form of lipids, which is used preferentially by muscle and other peripheral tissues over glucose because of insulin resistance [34].…”

Mechanisms and consequences of intestinal dysbiosis

“…A high-protein diet increases the production of branched-chain fatty acids, but also the production of potentially toxic substances such as sulfide, ammonia and N-nitroso compounds [27,39,41]. With an excess dietary intake of protein and amino acids, also the synthesis of nitric oxide increases [42]. This antimicrobial product strongly influences the gut microbiota, and increased NO levels measured in obese patients likely contribute to the development of an obesity-associated microbiota [42][43][44].…”

“…With an excess dietary intake of protein and amino acids, also the synthesis of nitric oxide increases [42]. This antimicrobial product strongly influences the gut microbiota, and increased NO levels measured in obese patients likely contribute to the development of an obesity-associated microbiota [42][43][44].…”

Metabolic Syndrome: A Multifaceted Disease of Affluence

“…This excess lipid is translated into hyperlipidemia/dyslipoproteinemia [16], with hy- pertriacylglycerolemia [17], hypercholesterolemia with altered lipoprotein distribution of cholesterol, and small dense LDLs [18]. An obvious consequence of excess lipid energy is a decrement in the overall carbohydrate availability [8] (lipid/carbohydrate energy ratio), which also affects the handling of dietary protein and the excretion of N [19]. This picture is completed by an increased proportion of oxidized lipoproteins in the plasma [20].…”

“…However, ammonium production, necessary for urea synthesis and thus N excretion, is limited by this same excess of energy as shown by lower urea excretion [65]. Consequently, patients with MS display excess N availability [19]. Because N does not accumulate in the body, it must be excreted.…”