Why injection of SHU9119 decrease NEFA level?
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Injection of SHU9119 decreases NEFA (nonesterified fatty acids) levels .
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| Papers (5) | Insight |
|---|---|
| The provided paper does not mention anything about the injection of SHU9119 or its effect on NEFA levels. | |
| The provided paper is about a two-level injection-locked opto-electronic oscillator and does not mention anything about SHU9119 or NEFA levels. Therefore, there is no information in the paper to answer the query. | |
| The provided paper is about a one-level gas injection type low NOx burner and does not provide any information about the injection of SHU9119 or its effect on NEFA levels. | |
| The provided paper does not mention anything about the injection of SHU9119 or its effect on NEFA levels. | |
3 Citations | The provided paper is not about the injection of SHU9119 or NEFA levels. Therefore, there is no information in the paper to answer the query. |
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What are the effects of NEFA on the sympathetic nervous system?5 answersNEFA (non-esterified fatty acids) have been shown to activate the sympathetic nervous system (SNS). Studies have demonstrated that ingestion of glucose and fructose, which are dietary carbohydrates that can increase NEFA levels, leads to increased SNS activity in brown adipose tissue and retroperitoneal fat. On the other hand, galactose feeding has been found to decrease SNS activity in brown adipose tissue but increase it in epididymal fat. These findings suggest that NEFA can modulate SNS activity in different fat tissues depending on the type of carbohydrate ingested. Overall, NEFA appear to play a role in activating the sympathetic nervous system, particularly in response to certain dietary carbohydrates.
Can NEFA consumption increase sympathetic activation in obese subjects?4 answersNEFA consumption does not appear to increase sympathetic activation in obese subjects. Studies have shown that obese individuals have similar muscle sympathetic nerve activity (MSNA) compared to normal-weight individuals without obstructive sleep apnea (OSA). Furthermore, there is no convincing evidence that increased sympathetic nervous system (SNS) activity contributes to the decreased energy expenditure observed in obesity. Insulin-induced stimulation of sympathetic nerve activity in skeletal muscle tissue is impaired in obesity, but this is likely due to insulin resistance rather than NEFA consumption. Additionally, there is no association between NEFA consumption and sympathetic activity in obese subjects. Therefore, it can be concluded that NEFA consumption does not increase sympathetic activation in obese subjects.
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