Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were carried out to test whether the ventromedial hypothalamus (VMH) is the site of a pathway that stimulates thermoregulatory heat production in brown adipose tissue (BAT). Adult Sprague-Dawley rats received bilateral 50 nl microinjections of colchicine solution into the VMH (0.1, 0.32, 1.0 or 3.2 micrograms per side). Beginning a day later, hyperphagia developed consistently with 0.32 microgram colchicine; and with higher doses there appeared the additional effect that for several days rats developed hypothermia when placed temporarily at 6 degrees C. The degree of hypothermia was limited by activation of nonshivering thermogenesis (NST) in BAT, as evidenced by increased shivering after propranolol injection to block NST, and by increased GDP binding measured in IBAT mitochondria after cold exposure. The findings suggest that chemical lesioning to induce the VMH hyperphagia syndrome does not produce an obligatory impairment of thermoregulation against cold unless the dose of neurotoxin and lesion area extends beyond that which underlies the overeating response. Furthermore, when tolerance to cold is thus compromised, the effect is not readily explained in terms of simply disconnecting a proposed stimulatory pathway from the VMH to BAT.
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PMID:Colchicine lesions of ventromedial hypothalamus: effects on regulatory thermogenesis in the rat. 273 41

Leptin contributes to the regulation of thermogenesis. In rodents, sympathetic nerve activity efferent to interscapular brown adipose tissue (IBAT-SNA) is involved. On the basis of the hypotheses that 1) leptin acutely potentiates hypothermia-induced increases in IBAT-SNA; 2) this action of leptin is specific to IBAT-SNA, i.e., it does not occur with renal sympathetic nerve activity (R-SNA); and 3) this effect of leptin depends on intact and functional leptin receptors, we measured IBAT-SNA and R-SNA in anesthetized lean and diet-induced obese Sprague-Dawley and in obese Zucker rats, randomly assigned to low-dose leptin or vehicle. Before the start of leptin or vehicle and 5 min, 90 min, and 180 min after, hypothermia (30 degrees C) was induced. Compared with vehicle, leptin did not significantly alter baseline R-SNA or IBAT-SNA. In lean Sprague-Dawley rats, hypothermia-induced increases in IBAT-SNA were significantly augmented by leptin but not by vehicle. In obese Sprague-Dawley rats, leptin did not potentiate hypothermia-induced increases in IBAT-SNA. In Zucker rats, IBAT-SNA did not increase with hypothermia and leptin was not able to induce sympathoactivation with cooling. Changes in R-SNA during hypothermia were not significantly modified by leptin in either group. Thus, low-dose leptin, although not altering baseline SNA, acutely enhances hypothermia-induced sympathetic outflow to IBAT in lean rats. This effect is specific for thermogenic SNA because leptin does not significantly alter the response of R-SNA to hypothermia. The effect depends on intact and functional leptin receptors because it occurs neither in rats with a leptin receptor defect nor in rats with acquired leptin resistance.
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PMID:Leptin potentiates thermogenic sympathetic responses to hypothermia: a receptor-mediated effect. 1214 55