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Organisms necessarily release heat energy in their pursuit of survival. This process is known as cellular thermogenesis and is implicated in many processes from cancer metabolism to spontaneous farm fires. However, the molecular basis for this fundamental phenomenon is yet to be elucidated. Here, we show that the major players involved in the cellular thermogenesis of Escherichia coli are the protein kinases ArcB, GlnL, and YccC. We also reveal the substrate-level control of adenosine triphosphate (ATP)-driven autophosphorylation that governs cellular thermogenesis. Specifically, through live cell microcalorimetry, we find these regulatory proteins, when knocked out in a model E. coli strain, dysregulate cellular thermogenesis. This dysregulation can be seen in an average 25% or greater increase in heat output by these cells. We also discover that both heat output and intracellular ATP levels are maximal during the late log phase of growth. Additionally, we show that microbial thermogenesis can be engineered through overexpressing glnL. Our results demonstrate a correlation between ATP concentrations in the cell and a cell's ability to generate excess heat. We expect this work to be the foundation for engineering thermogenically tuned organisms for a variety of applications., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2023 Dhatt et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

1. Sixty marasmic children were investigated for the absorption of xylose, proteins and fats. Their duodenal juice samples were also analysed for bile salts and microflora. 2. The marasmic children were then studied in three groups of twenty by allocating them to three different dietary schedules: a high-protein diet (30% of the total energy from protein), a high-fat diet (40% of the total energy from fat) and a high-carbohydrate diet (70% of the total energy from carbohydrate) for 2 weeks and the previous measurements repeated. 3. Whereas the high-fat diet resulted in improved fat absorption, along with an increase in total and conjugated bile acids, and the high-carbohydrate diet led to improved xylose absorption, the diet rich in protein resulted in an improvement in the absorption of all three dietary ingredients. It appears that a high-protein diet improves the overall absorption process by improving the intestinal environment as a whole, while high-carbohydrate and high-fat diets bring about adaptive changes related to the respective absorptive processes.

1. Plasma tyrosine and urinary p-hydroxyphenyl lactic acid (PHPLA) and p-hydroxyphenyl acetic acid (PHPAA) were studied in thirty patients with marasmus and twenty normal controls in the same age group. 2. In the control group conventional tyrosyluria was not observed but 30% of the group excreted high levels of PHPAA. In the group with marasmus, plasma tyrosine and urinary PHPLA and PHPAA values were signigificantly higher than the control values. However only 13.3% of the patients were considered to have conventional tyrosyluria and 52.3% were found to excrete high levels of PHPAA. 3. Administration of ascorbic acid resulted in a reduction of PHPLA excretion while it had no effect on PHPAA excretion. 4. It was inferred that (a) tyrosyluria in marasmus is due to the reduced activity of the hepatic enzyme 4-hydroxyphenyl pyruvate: oxygen oxidoreductase (hydroxylating, decarboxylating) (PHPAA-oxidase; EC 1.13.11.27) due to the deficiency of ascorbic acid and (b) high excretion of PHPAA is related to age and nutrition of the child and is unaffected by the administration of ascorbic acid. 5. It was further inferred that urinary excretion of PHPLA is a reliable index of tyrosyluria.

Sixty marasmic children and fifteen normal age-matched controls were investigated for the absorption of fats and proteins. Their duodenal juice samples were also analysed for bile salts and microflora. A significant amount of malabsorption, with respect to both the dietary ingredients, was observed in the majority of the marasmic children. The levels of conjugated bile acids in the duodenal juice samples of marasmic children were significantly lower as compared with those of normal controls, while the reverse was true for free bile acids and bacterial counts. Significant correlations were observed between bile acid levels and fat absorption and also between microflora and free bile acids. The pathophysiology of malabsorption in marasmus is discussed in the light of these findings.