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but cvos releases prostaglandins that reset the hypothalamic set point upward, unless it's countered by anti-pyretic therapy.
لكن الجهاز البطيني يطلق البروستاجلاندين الذي يرفع النقطة الهيبوتلاموسية إلا إن عارضه علاج مضاد للحمى
hbcd has a potential to interfere with the hypothalamic-pituitary-thyroid (hpt) axis and cause reproductive and developmental effects.
ولهذه المادة قدرة على التداخل مع محور هرمونات الهايبوثلامس والغدتين النخامية والدرقية مسببة تأثيرات على الإنجاب والنمو.
2 hedonic response to sugar and rewards of sugar intake while the hypothalamus regulates food intake in terms of energetic needs, the dopamine reward/motivation circuitry involving striatal, limbic and cortical areas also drives eating behavior (28). other neurotransmitters including serotonin, endogenous opioids, and endocannabinoids confer the rewarding effects of food in part by modulating its hedonic properties (29). ingestion of palatable food releases dopamine (da) in the ventral and dorsal striatum and dorsal striatal da release is proportional to the self- reported level of pleasure gained by eating the food (30). highly palatable foods, namely those rich in sugar or fat, can strongly trigger these reward/motivation and hedonic systems, encouraging food intake beyond the necessary energy requirements (31). while this may have been evolutionarily advantageous by encouraging fat storage when food was scarce, overeating becomes a liability in our current environment, which has no shortage of highly caloric and processed foods. there are two principal rewarding aspects of sugar consumption: nutrition and taste. rodent studies have indicated that these two aspects are distinct and dissociable and may follow different neural pathways (32,33). one path for the nutritive rewards of sugar comes from melanin-concentrating hormone (mch) neurons in the lateral hypothalamus (32). in rodents, these neurons fire in response to extracellular glucose levels, independent of gustatory input, and project to dopamine neurons in the midbrain that in turn project to the ventral and dorsal striatum. though animals typically prefer sucrose over sucralose (non-nutritive sweetener), transgenic mice who lack mch neurons do not, showing that this pathway is essential for encoding nutritive reward. when mch neurons are optogenetically stimulated during the consumption of sucralose, the mouse brain is tricked into responding as if it is receiving caloric energy with a resultant increase in striatal da and even preference of sucralose over sucrose (32). the nutritive reward value of sugar is associated with increases in da release in the dorsal striatum (34). when infused intra-gastrically in mice to avoid the confounds of taste, glucose elicited da release in the dorsal striatum while sucralose did not (34). the sweet taste of sugar is also rewarding— offering an explanation as to why artificial sugars like sucralose are still consumed despite their lack of nutritive value. the reward of the sweet taste, however, activates a different neural pathway than the caloric input. while the nutritive reward of sugar in mice causes da release primarily in the dorsal striatum, the sweetness reward is concentrated in the ventral striatum (32). consumption of sucralose in mice was associated with increased da in the ventral striatum except when tainted by a bitter additive, suggesting that the reward is derived from the palatable taste rather than another feature of sucralose (34). although both the nutritive and taste rewards of sugar are, to some extent, neurologically distinct, they occur in tandem and are interrelated. a recent study showed that mice modified to have disrupted da d-2 receptor (drd2) signaling in the nucleus accumbens (nac) shell of the ventral striatum exhibited more perseverative and impulsive sucrose-taking, increased sucrose reinforcement, increased reinforcement/ reward learning of glucose-paired flavors, and worsened learning flexibility (35). additionally, these mice were less efficient in metabolizing glucose. this suggests that drd2 in the nac are essential both for regulating peripheral glucose levels as well as the reinforcement/reward learning of glucose consumption (35), which explains why dysregulation of this system may lead to overeating. 3.3 hedonic response: fructose vs. glucose just as fructose and glucose have different metabolic pathways, they have different hedonic effects on the brain and behavior. fifteen minutes after subjects received a drink of either pure fructose or glucose during a functional mri (fmri) scan, those receiving glucose showed a significantly reduced amount of cerebral blood flow (cbf) in the hypothalamus, insula, anterior cingulate cortex, and striatum when compared to baseline (17). they also showed greater functional connectivity between the hypothalamus, thalamus, caudate, and putamen. the increased connectivity between the hypothalamus and the dorsal striatum after glucose was interpreted to reflect engagement of the nutritive reward pathway. the reduction in hypothalamic activity and increased connectivity with reward centers was accompanied by a perceived increase in fullness and satiety. in contrast, consuming a fructose drink was not associated with reduced cbf in the hypothalamus, but instead with reduced cbf in the thalamus, hippocampus, posterior cingulate cortex, fusiform gyrus, and visual cortex. although those in the fructose group did have increased connectivity between the thalamus and hypothalamus, there was no increase detected with the dorsal striatum as observed in the glucose group. correspondingly, fructose consumption did not significantly reduce hunger. fructose consumption has also been associated with a stronger fmri response in the visual cortex to high calorie foods compared that with glucose consumption (14). as fructose delivers a sweet taste without an immediate nutritive input, it follows that fructose consumption should be associated with increased appetitive behavior and reactivity to food. 3.4 sugar and addiction sugar has been
