ABSTRACT
<p><b>OBJECTIVES</b>To examine the effects of β(3)-adrenergic receptor gene polymorphism on body weight change during a weight reduction program for middle-aged, overweight women with careful consideration of their energy intake and expenditure.</p><p><b></b>METHODS</p><p><b>DESIGN</b>Intervention study of weight reduction for 12 weeks in a community setting.</p><p><b>SUBJECTS</b>Eighty overweight middle-aged women who completed the individualized lifestyle modification program.</p><p><b>MEASUREMENTS</b>β(3)-adrenergic receptor gene polymorphism was identified by polymerase chain reaction and consecutive restriction fragment-length polymorphism analysis. Anthropometrical parameters, lifestyle factors, blood lipid and glucose levels, physical activity level and energy intake were measured before and at the end of the program.</p><p><b>RESULTS</b>The numbers of subjects with the Trp64Trp, Trp64Arg, and Arg64Arg genotypes were 45, 30 and 5, respectively. Baseline characteristics among subjects with the 64Arg allele had significantly smaller decrease in body weight and energy intake than those without the 64Arg allele. The change of other clinical characteristics did not differ between the two groups. After adjusting for the %change of energy intake, the %change of body weight did not differ between the two groups.</p><p><b>CONCLUSION</b>The 64Arg allele of the β(3)-AR gene is not likely to be the factor determining the difficulty in losing body weight in Japanese middle-aged, overweight women. Lifestyle factors, such as the decrease in energy intake, might mask the effect of the 64Arg allele on body weight loss. Specific considerations for the management of energy intake would be needed to promote body weight loss for those with the 64Arg allele.</p>
ABSTRACT
Objectives: To examine the effects of β3-adrenergic receptor gene polymorphism on body weight change during a weight reduction program for middle-aged, overweight women with careful consideration of their energy intake and expenditure. Methods: Design: Intervention study of weight reduction for 12 weeks in a community setting. Subjects: Eighty overweight middle-aged women who completed the individualized lifestyle modification program. Measurements: β3-adrenergic receptor gene polymorphism was identified by polymerase chain reaction and consecutive restriction fragment-length polymorphism analysis. Anthropometrical parameters, lifestyle factors, blood lipid and glucose levels, physical activity level and energy intake were measured before and at the end of the program. Results: The numbers of subjects with the Trp64Trp, Trp64Arg, and Arg64Arg genotypes were 45, 30 and 5, respectively. Baseline characteristics among subjects with the Trp64Trp, Trp64Arg and Arg64Arg alleles did not differ. After 12 weeks, the subjects with the 64Arg allele had significantly smaller decrease in body weight and energy intake than those without the 64Arg allele. The change of other clinical characteristics did not differ between the two groups. After adjusting for the %change of energy intake, the %change of body weight did not differ between the two groups. Conclusion: The 64Arg allele of the β3-AR gene is not likely to be the factor determining the difficulty in losing body weight in Japanese middle-aged, overweight women. Lifestyle factors, such as the decrease in energy intake, might mask the effect of the 64Arg allele on body weight loss. Specific considerations for the management of energy intake would be needed to promote body weight loss for those with the 64Arg allele.
Subject(s)
Energy Intake , Body Weight , Obesity , Alleles , Receptors, AdrenergicABSTRACT
BACKGROUND: Body temperature is usually regulated by opposing controls of heat production and heat loss. However, systemic administration of capsaicin, the pungent ingredient of hot peppers, facilitated heat production and heat loss simultaneously in rats. We recently found that the capsaicin-induced heat loss and heat production occur simultaneously and that the biphasic change in body temperature is a sum of transient heat loss and long-lasting heat production. Moreover, suppression of the heat loss response did not affect capsaicin-induced heat production and suppression of heat production did not affect capsaicin-induced heat loss. These observations suggest the independent peripheral mechanisms of capsaicin-induced thermal responses. Thus, the capsaicin-induced thermal responses apparently lack an integrated control. METHODS: Male Wistar rats were maintained at an ambient temperature of 24 1 degrees C on a 12 h on-off lighting schedule at least for two weeks before the experiments. They were anesthetized with urethane (1.5 g/kg, i.p.) and placed on a heating pad, which was kept between 29 and 30 degrees C. Skin temperature(Ts) was measured with a small thermistor, which was taped to the dorsal surface of the rat's tail, to assess vasoactive changes indirectly. Colonic temperature(Tc) was measured with another thermistor inserted about 60 mm into the anus. O2 consumption was measured by the open-circuit method, and values were corrected for metabolic body size (kg0.75). Capsaicin (Sigma) was dissolved in a solution comprising 80+ACU- saline, 10+ACU- Tween 80, and 10+ACU- ethanol, and injected subcutaneously at a dose of 5 mg/kg. Each rat received a single injection of capsaicin because repeated administration of capsaicin renders an animal insensitive to the subsequent administration of capsaicin. Laminectomy was performed at the level of the first and second cervical vertebrae to expose the cervical spinal cord for sectioning. The brain was transected at 4-mm rostral from the interaural line with an L-shaped knife. RESULTS: After administration of capsaicin, O2 consumption increased from 13.5 0.4 mL/min/kg0.75 at 0 min to a peak of 15.9 0.4 mL/min/kg0.75 at 71 min and gradually declined but remained higher than the basal value until the end of the 4-h observation period. Ts also immediately increased from 27.7 0.2 degrees C to 31.9 0.3 degrees C at 39 min, and it returned to the baseline level within 90 min after the capsaicin administration. Tc initially decreased from 37.1 0.1 degrees C to 36.8 0.2 degrees C at 43 min and then gradually increased over the baseline level and remained at 37.6 0.2 degrees C until the end of the experiment. In spinalized rats, the capsaicin-induced increases in O2 consumption was largely attenuated, while the basal O2 consumption was similar to that of control rats. The basal Ts of spinalized rats was 32.4 0.3 degrees C, which was higher than that of control rats. Capsaicin increased Ts by less than 1 degree C, and Tc did not change after the capsaicin administration. O2 consumption of decerebrated rats was statistically higher than that of control rats after the injection of capsaicin. However, capsaicin did not increase Ts, showing a lack of a vasodilatory response. Decerebration between the hypothalamus and midbrain prevented the capsaicin-induced heat loss but not the heat production response. CONCLUSION: These results show that the capsaicin-induced heat production and heat loss are controlled separately by the brainstem and by the forebrain, respectively, and suggest that the body temperature regulation is performed without an integrative center.
Subject(s)
Male , Rats , Animals , Body Temperature Regulation , Brain/physiology , Brain/drug effects , Capsaicin , Decerebrate State , Oxygen Consumption/drug effects , Rats, WistarABSTRACT
Objective: To investigate how fatty liver was developed in ventromedial hypothalamus(VMH)-lesioned obese rats. Methods: Two groups of rats were prepared: (1)VMH-lesioned obese rats, and (2)sham VMH-lesioned rats. One week after VMH lesions, livers of all rats were isolated for morphological observation and for determination of microsomal triglyceride transfer protein(MTP), phosphatidate phyosphohydrolase (PAP), malic enzyme (ME), and glucose-6-phosphate dehydrogenase(G6PDH). Results: Triglyceride contents in livers of VMH-lesoned obese rats increased significantly, and were about 1.8-fold of control group. Activities of ME, G6PDH and PAP in the livers were also enhanced markedly compared to their controls. Many lipid droplets in cytoplasm of hepatocytes from VMH-lesioned obese rats were observed, while there was no similar finding in hepatocytes of control rats. MTP activity in livers of VMH-lesioned obese rats was higher than that in livers of sham-operated non-obese rats [0.201?0.013 vs. 0.175?0.014 ?g/(mg protein?h),[WTBX]P0.05). Conclusion: Hepatic triglyceride production and activity of MTP were increased in VMH-lesioned obese rats, but magnitude of the latter did not exceed the former. This resulted in hepatic triglyceride accumulation in spite of increase in transport of triglyceride out of liver by MTP. This may contribute to the development of fatty liver in VMH-lesioned obese rats.
ABSTRACT
Objective: To investigte the lipogenic and lipolytic metabolism at dynamic phase of obesity in ventromedial hypothalamus-lesioned obese rats. Methods: Female SD rats were divided into two groups, one group received bilateral electrolytic lesions of ventromedial hypothalamus(VMH),and the other one was used as sham control. Samples of blood, livers and subcutaneous, parametric and mesenteric adipose tissues were collected one week after VMH lesions and sham operations. Results: Activities of microsomal triglyceride transfer protein(MTP) in hepatocytes, and phosphatidate phosphohydrolase (PAP), malic enzyme(ME), glucose-6-phosphate dehydrogenase(G6PDH)in liver, parametric and mesenteric adipose tissue in VMH-lesioned rats were increased as compared to their sham counterparts. Activity of hormone sensitive enzyme(HSL) in parametric and mesenteric adipose tissue in VMH-lesioned rats was not changed when compared to sham group. Activity of HSL in subcutaneons adipose tissue was increased, while activity of HSL in gastrocnemius was decreased. Activity of lipoprotein lipase(LPL) in parametric and mesenteric adipose tissue and gastrocnemius were enhanced significantly compared to sham group. Conclusion: In dynamic phase of obesity of VMH-lesioned rats, hepatic production and transportation of triglyceride in these rats were increased significantly ,and lipogenic metabolism and storage of triglyceride in adipose tissues such as parametric and mesenteric adipose tissues were also enhanced.Meanwhile, lipolytic metabolism in subcutaneous adipose tissue and gastrocnemius was also increased.
ABSTRACT
Objective: To investigate the effects of peripheral leptin infusion on metabolism in ventromedial hypothalamus (VMH) lesioned obese rats. Methods: Four groups were prepared: (1) VMH lesioned rats with infusion of leptin, (2) VMH lesioned rats with infusion of saline, (3) sham VMH lesioned rats with infusion of leptin and (4) sham VMH lesioned rats with infusion of saline. After VMH lesion and sham operations, a mini pump filled with either leptin or saline was implanted into the back of rats. Body weight and food intake were recorded daily. Seven days later, all rats were sacrificed after overnight fast. Blood samples were collected for determination of glucose, triglyceride, total cholesterol, insulin and leptin. Perimetric fat pad (PFD) was isolated and weighed. Pancreas was embedded by paraffin and sectioned, and performed by immunostaining with proliferating cell nuclear antigen (PCNA) for study of the proliferative activity of insular cells. Results: In sham operated groups, food intake and increased body weight decreased significantly in rats with leptin infusion than those without leptin infusion. No similar findings were observed in VMH lesioned rats. Plasma insulin, triglyceride and total cholesterol in the rats with leptin infusion regardless of VMH lesion or sham operations were decreased when compared with their controls. In respect to PFD, two VMH lesioned groups did not differ, but two sham operated groups differed. Positive PCNA rate in VMH lesioned rats receiving leptin declined significantly. Conclusion: Leptin regulations of food intake, body weight and body fat are dependent upon intact VMH. Peripheral infusion of leptin decreases plasma triglyceride and total cholesterol in VMH lesioned rats.