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Regional variation in leptin-induced sympathoactivation in agouti obese mice
AJH–May 2004 –VOL. 17, NO. 5, PART 2
POSTERS: Obesity, Insulin Resistance, Diabetes
from that in the NHANES population in two respects (Figure 1): the prevalence of MetS in the veteran population was much higher, and it declined markedly after age 60. In 7/2002 a Metabolic Syndrome Clinic (MSC) was established to provide systematic managment of these pateints to lower their CHD risk. Patients are seen monthly for 6 visits in the multidisiplinary clinic, with assessment of lipid levels, glucose, vital signs and diet and exercise regimens. Goals of therapy are LDL⬍100, non-HDL⬍130, TG⬍150, BP⬍130/80. Since 7/2002 and 10/2003, 378 patients have been discharged from the MSC clinic. During the brief intervention period, benificial changes have been noted in lipids, glucose, and blood pressure (Table 1). The changes in lipids and blood pressure are striking. MetS appears particuliarly important in the veteran population. The decline in MetS prevalence after age 60, suggesting premature CHD mortality, indicates that this population is at high risk and warrants aggressive managment. We conclude that MetS cardiovascular risk factors can be improved rapidly by a focused intervention.
217A
diabetic therapy. BP was the mean of 5 measurements using an automatic BP device (Omron digital automatic blood pressure monitor). The exercise protocol, as shown in the table, induced a statistically significant decrease of the mean blood pressure, fasting glucose, HbA1c and frutosamine, but no changes on the weight or the level of total cholesterol of the active group when compared with the control group. A significant positive correlation was found between the effect of the exercise on the systolic BP and on weight (r⫽0,45 p⬍0,05) and a negative correlation between the effect of exercise on systolic blood pressure and HbA1c (r⫽-0,36 p⬍ 0,05). We concluded that even a relative short time protocol of regular exercise induces a beneficial effect on type II diabetic patients decreasing blood pressure and allowing a better control of blood glucose levels. Ageyrs Active group (23) Baseline Control group (10) Baseline ƒ Active-posexercise (a) ƒ Control group 3 months later (b) p, a v b
Weight Kg
MBPmm Hg
Fasting glucose
Hb A1C %
Frutosamine T-Chol
53 ⫾ 9
77 ⫾ 13
97 ⫾ 9
10.2 ⫾ 5.0
9.1 ⫾ 3.0
417 ⫾ 140
4.6 ⫾ 1.0
55 ⫾ 8
81 ⫾ 15
103 ⫾ 10
9.9 ⫾ 8.0
8.9 ⫾ 4.0
378 ⫾ 167
5⫾1
⫾
⫹0.4 ⫾ 2.0
⫺4 ⫾ 7
⫺0.6 ⫾ 4
⫺1.3 ⫾ 2.0
⫺66 ⫾ 171
⫹0.1 ⫾ 1.0
⫹1.3 ⫾ 2.0
⫹0.9 ⫾ 2
⫹3.8 ⫾ 5
⫺0.03 ⫾ 1.0
⫹144 ⫾ 225
⫹0.8 ⫾ 1.0
ns
0.012
0.03
0.02
0.05
ns
Key Words: Diabetes, Exercise, Blood Pressure
Table 1. Metabolic syndrome characteristics improve rapidly Parameter
Average at Average Last Change from baseline Visit 1 Visit (%)
Blood Pressure (mmHg) 135/78 Weight (lbs) 353 pts 217 Waist (inches) 208 pts 43.76 Tot Chol (mg/dL) 372 pts 200 Triglycerides (mg/dL) 371pts 187 LDL (mg/dL) 371pts 122 HDL (mg/dL) 371pts 42.2 Non-HDL 157 Glucose (mg/dL) 359pts 118
127/74 215 43.23 171 134 98 45.4 125 108
⫺8/⫺4 (⫺6/⫺6) ⫺2 (⫺0.8) ⫺0.53 (⫺1.2) ⫺29 (⫺15) ⫺53 (⫺29) ⫺24 (⫺19) ⫹3.2 (⫹7.5) ⫺32 (⫺20) ⫺10 (⫺8)
Key Words: Metobolic Syndrome, Coronary Heart Disease Risk, Insulin Resistance
P-504 THE EFFECT OF A REGULAR EXERCISE PROGRAM IN THE CONTROL OF BLOOD PRESSURE AND PLASMA GLUCOSE LEVELS IN TIPE II SEDENTARY DIABETIC PATIENTS Albertino Damasceno, Paula Caupers, Antonio Prista, B Fernhaall, B Chemane, O Pateguane, Jorge Polonia. Department of Medicine and Exercise Physiology Laboratory, Faculty of Medicine, Eduardo Mondlane University, Maputo, Mozambique; Physiology Laboratory of the Syracuse University., Syracuse University., , South Africa; UN Farmacol Clinica, Faculdade Medicina Porto, Porto, Portugal. We analyzed the effect of a three months protocol of regular and controlled exercise (1 hour/day, 3 to 5 days a week at a level between 50 to 75% of the previously determined VO2Max), on the Weight, Resting Blood Pressure (BP), Total and HDL Cholesterol, Glycosilated Hemoglobin, Frutosamine and Fasting Blood Glucose of 23 type II previously sedentary diabetic male patients compared with a control group of 10 type II male sedentary diabetic patients. Patients were analyzed in the beginning and immediately after the 3 months period of the protocol exercise (Active Group) or maintaining the usual lifestyle (Control Group) without any change of the previous anti-hypertensive and anti
P-505 REGIONAL VARIATION IN LEPTIN-INDUCED SYMPATHOACTIVATION IN AGOUTI OBESE MICE Kamal Rahmouni, William G Haynes, Donald A Morgan, Gina M Morgan, Marcelo LG Correia, Allyn L Mark. Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA. We have previously demonstrated that in agouti obese mice there is selective resistance to leptin with preservation of the renal sympathetic nerve activity (SNA) response to leptin despite loss of the feeding- and weight-reducing effects of leptin. Because only the renal SNA response to leptin was examined in these studies, it was not clear if leptin-induced sympathoactivation to other beds was preserved or lost in this model of obesity with leptin resistance. In this study, we tested the hypothesis that in agouti obese mice while the renal SNA response to leptin is preserved, the SNA response to other beds may be impaired. For this, we compared the brown adipose tissue (BAT) and lumbar SNA responses to intravenous administration of vehicle and leptin (60 and 120 g) in anesthetized lean and agouti obese mice. In lean mice, intravenous administration of leptin caused a dose-dependent rise in both BAT and lumbar SNA. Leptin (120 g) increased BAT and lumbar SNA by 187⫾37% (n⫽8, P⬍0.001 vs. vehicle) and 100⫾31 (n⫽8, P⬍0.001), respectively. In contrast, agouti obese mice had a significantly attenuated (P⬍0.05 vs. lean mice) BAT and lumbar sympathoactivation to leptin. In these obese mice, 120 g of leptin increased BAT and lumbar SNA by only 84⫾29% (n⫽8) and 4⫾24% (n⫽8), respectively. Preservation of leptin-induced sympathoactivation in agouti obese mice appears to be specific to the renal SNA because the BAT and lumbar SNA are resistant to leptin in this model of obesity. Loss of thermogenic sympathoactivation to leptin may promote obesity while preservation of renal sympathoactivation to leptin in presence of hyperleptinemia may promote hypertension. Key Words: Leptin resistance, sympathetic Nerve Activity, Hypertension
POSTERS: Obesity, Insulin Resistance, Diabetes
from that in the NHANES population in two respects (Figure 1): the prevalence of MetS in the veteran population was much higher, and it declined markedly after age 60. In 7/2002 a Metabolic Syndrome Clinic (MSC) was established to provide systematic managment of these pateints to lower their CHD risk. Patients are seen monthly for 6 visits in the multidisiplinary clinic, with assessment of lipid levels, glucose, vital signs and diet and exercise regimens. Goals of therapy are LDL⬍100, non-HDL⬍130, TG⬍150, BP⬍130/80. Since 7/2002 and 10/2003, 378 patients have been discharged from the MSC clinic. During the brief intervention period, benificial changes have been noted in lipids, glucose, and blood pressure (Table 1). The changes in lipids and blood pressure are striking. MetS appears particuliarly important in the veteran population. The decline in MetS prevalence after age 60, suggesting premature CHD mortality, indicates that this population is at high risk and warrants aggressive managment. We conclude that MetS cardiovascular risk factors can be improved rapidly by a focused intervention.
217A
diabetic therapy. BP was the mean of 5 measurements using an automatic BP device (Omron digital automatic blood pressure monitor). The exercise protocol, as shown in the table, induced a statistically significant decrease of the mean blood pressure, fasting glucose, HbA1c and frutosamine, but no changes on the weight or the level of total cholesterol of the active group when compared with the control group. A significant positive correlation was found between the effect of the exercise on the systolic BP and on weight (r⫽0,45 p⬍0,05) and a negative correlation between the effect of exercise on systolic blood pressure and HbA1c (r⫽-0,36 p⬍ 0,05). We concluded that even a relative short time protocol of regular exercise induces a beneficial effect on type II diabetic patients decreasing blood pressure and allowing a better control of blood glucose levels. Ageyrs Active group (23) Baseline Control group (10) Baseline ƒ Active-posexercise (a) ƒ Control group 3 months later (b) p, a v b
Weight Kg
MBPmm Hg
Fasting glucose
Hb A1C %
Frutosamine T-Chol
53 ⫾ 9
77 ⫾ 13
97 ⫾ 9
10.2 ⫾ 5.0
9.1 ⫾ 3.0
417 ⫾ 140
4.6 ⫾ 1.0
55 ⫾ 8
81 ⫾ 15
103 ⫾ 10
9.9 ⫾ 8.0
8.9 ⫾ 4.0
378 ⫾ 167
5⫾1
⫾
⫹0.4 ⫾ 2.0
⫺4 ⫾ 7
⫺0.6 ⫾ 4
⫺1.3 ⫾ 2.0
⫺66 ⫾ 171
⫹0.1 ⫾ 1.0
⫹1.3 ⫾ 2.0
⫹0.9 ⫾ 2
⫹3.8 ⫾ 5
⫺0.03 ⫾ 1.0
⫹144 ⫾ 225
⫹0.8 ⫾ 1.0
ns
0.012
0.03
0.02
0.05
ns
Key Words: Diabetes, Exercise, Blood Pressure
Table 1. Metabolic syndrome characteristics improve rapidly Parameter
Average at Average Last Change from baseline Visit 1 Visit (%)
Blood Pressure (mmHg) 135/78 Weight (lbs) 353 pts 217 Waist (inches) 208 pts 43.76 Tot Chol (mg/dL) 372 pts 200 Triglycerides (mg/dL) 371pts 187 LDL (mg/dL) 371pts 122 HDL (mg/dL) 371pts 42.2 Non-HDL 157 Glucose (mg/dL) 359pts 118
127/74 215 43.23 171 134 98 45.4 125 108
⫺8/⫺4 (⫺6/⫺6) ⫺2 (⫺0.8) ⫺0.53 (⫺1.2) ⫺29 (⫺15) ⫺53 (⫺29) ⫺24 (⫺19) ⫹3.2 (⫹7.5) ⫺32 (⫺20) ⫺10 (⫺8)
Key Words: Metobolic Syndrome, Coronary Heart Disease Risk, Insulin Resistance
P-504 THE EFFECT OF A REGULAR EXERCISE PROGRAM IN THE CONTROL OF BLOOD PRESSURE AND PLASMA GLUCOSE LEVELS IN TIPE II SEDENTARY DIABETIC PATIENTS Albertino Damasceno, Paula Caupers, Antonio Prista, B Fernhaall, B Chemane, O Pateguane, Jorge Polonia. Department of Medicine and Exercise Physiology Laboratory, Faculty of Medicine, Eduardo Mondlane University, Maputo, Mozambique; Physiology Laboratory of the Syracuse University., Syracuse University., , South Africa; UN Farmacol Clinica, Faculdade Medicina Porto, Porto, Portugal. We analyzed the effect of a three months protocol of regular and controlled exercise (1 hour/day, 3 to 5 days a week at a level between 50 to 75% of the previously determined VO2Max), on the Weight, Resting Blood Pressure (BP), Total and HDL Cholesterol, Glycosilated Hemoglobin, Frutosamine and Fasting Blood Glucose of 23 type II previously sedentary diabetic male patients compared with a control group of 10 type II male sedentary diabetic patients. Patients were analyzed in the beginning and immediately after the 3 months period of the protocol exercise (Active Group) or maintaining the usual lifestyle (Control Group) without any change of the previous anti-hypertensive and anti
P-505 REGIONAL VARIATION IN LEPTIN-INDUCED SYMPATHOACTIVATION IN AGOUTI OBESE MICE Kamal Rahmouni, William G Haynes, Donald A Morgan, Gina M Morgan, Marcelo LG Correia, Allyn L Mark. Hypertension Genetics SCOR, CV Center and Department of Internal Medicine, University of Iowa, Iowa City, IA. We have previously demonstrated that in agouti obese mice there is selective resistance to leptin with preservation of the renal sympathetic nerve activity (SNA) response to leptin despite loss of the feeding- and weight-reducing effects of leptin. Because only the renal SNA response to leptin was examined in these studies, it was not clear if leptin-induced sympathoactivation to other beds was preserved or lost in this model of obesity with leptin resistance. In this study, we tested the hypothesis that in agouti obese mice while the renal SNA response to leptin is preserved, the SNA response to other beds may be impaired. For this, we compared the brown adipose tissue (BAT) and lumbar SNA responses to intravenous administration of vehicle and leptin (60 and 120 g) in anesthetized lean and agouti obese mice. In lean mice, intravenous administration of leptin caused a dose-dependent rise in both BAT and lumbar SNA. Leptin (120 g) increased BAT and lumbar SNA by 187⫾37% (n⫽8, P⬍0.001 vs. vehicle) and 100⫾31 (n⫽8, P⬍0.001), respectively. In contrast, agouti obese mice had a significantly attenuated (P⬍0.05 vs. lean mice) BAT and lumbar sympathoactivation to leptin. In these obese mice, 120 g of leptin increased BAT and lumbar SNA by only 84⫾29% (n⫽8) and 4⫾24% (n⫽8), respectively. Preservation of leptin-induced sympathoactivation in agouti obese mice appears to be specific to the renal SNA because the BAT and lumbar SNA are resistant to leptin in this model of obesity. Loss of thermogenic sympathoactivation to leptin may promote obesity while preservation of renal sympathoactivation to leptin in presence of hyperleptinemia may promote hypertension. Key Words: Leptin resistance, sympathetic Nerve Activity, Hypertension