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TIFR researchers have discovered that the molecular anticipation of diet in the liver is essential to ensure that the body, after fasting, adapts to the use of incoming nutrients during re-feeding. Their conclusions, published in the international journal Cell reports, show that very small molecules of RNA, called microRNAs, control the main metabolic pathways by inhibiting protein synthesis and thus contribute to the maintenance of glucose levels in the blood.
The liver is one of the central metabolic organs that plays a vital role in maintaining the health and life of the body. All living organisms undergo fasting cycles, in which, generally, fats are broken down to meet energy needs, while glucose or carbohydrates are the main source of energy after eating. The inflexibility of oscillating between these processes stems from the inability of organs (or organisms) to change metabolic pathways. Overuse or underuse of lipids or glucose is known to affect the health of all life forms. In highly evolved species, the liver plays the major role in regulating the metabolism of lipids and glucose and avoiding the overuse or underuse of these sources of energy. Hepatic dysfunction is known to be badociated with obesity and diabetes. Abnormal liver metabolism is one of the major factors of fatty liver disease, which is widespread, especially among Indians. Thus, the molecular mechanisms within liver cells that result in a global change in gene expression from a fasting state to a closed state become critical. Scientists all over the world have recently stepped up their efforts to discover molecular factors that respond to food consumption (including the time of day) and circadian rhythm (light-dark cycles), particularly in the liver, and affect the body's overall metabolism.
The essential aspect of the research conducted at TIFR is the identification of "micro-RNA fed" – as their level increases in the liver after feeding – stopping the production of necessary protein during fasting. Although microRNAs are known to be important for liver functions, the recent discovery shows that a specific group of these small RNAs act together to curb the fasting response during a new diet. The salient point of the study is the discovery that the precursors of these microRNAs fed are already made when the mice are fasting, which creates a mechanism of anticipation. It is important to note that disruption of these fed microRNAs leads to molecular and physiological changes badociated with an badociated increase in blood glucose, recalling a prediabetic state. This study paves the way for the use of these small RNA molecules as potential therapeutic targets for controlling glucose or lipid metabolism and as a plausible intervention in metabolic (hepatic) diseases.
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