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The battle between fat and sugar: Who controls our energy metabolism?
In our diet, fat and sugar are the two main sources of energy, but the competition between their metabolism is an intricate process. Based on biochemical basis, this competitive relationship not only affects our energy levels, but can also lead to a range of health problems, such as type 2 diabetes and insulin resistance. This article will delve into this complex metabolic process and try to answer: Is fat or sugar controlling our energy metabolism?
"Randle cycle, also known as glucose-fatty acid cycle, is a metabolic process involving mutual inhibition between glucose and fatty acids."
Randle loop: foundation and mechanism
First described by Philip Randle in 1963, the Randle cycle is the basic metabolic pathway that cells follow when using different energy sources. In the Randle cycle, there is a competition between fatty acids and glucose. In the fasting state, fatty acids are preferentially used as an energy source, while after eating, especially after high-fat meals, glucose utilization is affected.
"The oxidation of fatty acids can inhibit glucose metabolism, and this phenomenon will be different in different stages of metabolism."
Metabolic changes in fed and fasted states
Fasted state
During fasting, the body uses fatty acids as its primary source of energy. The liver meets local energy needs by beta-oxidizing fatty acids, possibly leading to the production of ketone bodies. These ketone bodies are then used by other tissues, while glucose oxidation is inhibited, allowing the preservation of pyruvate and lactate, the precursors of glycogenesis.
Eating status
After eating, especially under the influence of a high-fat meal, the concentration of fatty acids or ketone bodies in the plasma will increase. At this time, unoxidized glucose is redirected to glycogen storage. This mechanism explains not only the rapid resynthesis of muscle glycogen after exercise but also the increased glycogen content in muscles during starvation or diabetic states.
"When the composition of the meal is in different proportions, although the overall energy balance is the same, the balance between glucose and fat will change with the proportion of the meal ingredients."
Metabolic inhibition mechanism
The short-term inhibition of glycolysis by fatty acid oxidation is achieved through multiple pathways, including the inhibition of pyruvate dehydrogenase, and mainly occurs at different stages of the glycolysis process. This inhibition relies on changes in the internal mitochondrial environment caused by fatty acid oxidation, such as an increase in the [acetyl-CoA]/[CoA] ratio, ultimately causing various stages of glucose metabolism to be affected. This process increases the accumulation of carboxylic acids, further inhibiting the conversion of endogenous sugars.
Hemodynamics and the role of AMPK
Under certain physiological conditions, such as hemodynamic stress, the body will preferentially metabolize glucose. During this period, substrate supply decreases and demand increases, prompting activation of AMPK to counteract the suppression of energy supply caused by fatty acids. The activation of AMPK not only provides an emergency metabolic adaptation mechanism for cells in a hypoxic state, but also protects the heart from damage caused by ischemia.
"During physiological stress, the balance between energy selection and substrate requirements is particularly important."
Oxidation mechanism of fatty acids and ketone body production
Malonyl-CoA plays an important signal transduction role in glucose utilization and long-chain fatty acid oxidation. When blood sugar rises, the concentration of Malonil-CoA increases, inhibiting the entry and oxidation of long-chain fatty acids. This means that the malonil-CoA produced by glucose helps promote the esterification of fatty acids, thereby affecting the overall metabolic trend.
Interaction and regulation of intracellular events
Intracellular enzyme systems, such as ACC and MCD, regulate the concentration of Malonil-CoA, which further affects the uptake and oxidation of fatty acids. When AMPK is activated, ACC is phosphorylated and inactivated, which reduces the concentration of Malonil-CoA, which in turn promotes fatty acid oxidation and ketone body production.
The effect of fatty acids on insulin
The presence of fatty acids not only affects energy selection, but also directly regulates glucose-stimulated insulin secretion in pancreatic beta cells. In the short term, fatty acids enhance the effects of glucose on insulin secretion, but in the long term, high concentrations of fatty acids cause inhibitory effects.
"In the presence of high fatty acid concentrations, Randle believes this creates a biochemical syndrome that affects all physiological responses based on carbohydrate metabolism."
Ultimately, how does the battle between fat and sugar affect our energy metabolism? What we are left to ponder will be how future research can provide more insights and understanding of this complex process.
