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Hypertension. 1996;27:125-129

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(Hypertension. 1996;27:125-129.)
© 1996 American Heart Association, Inc.


Articles

Decrease in Intra-Abdominal Visceral Fat May Reduce Blood Pressure in Obese Hypertensive Women

Hideyuki Kanai; Katsuto Tokunaga; Shigenori Fujioka; Shizuya Yamashita; Kaoru Kameda-Takemura; Yuji Matsuzawa

From The Division of Internal Medicine, Toyonaka Municipal Hospital (H.K.), and The Second Department of Internal Medicine, Osaka (Japan) University Medical School.

Correspondence to Hideyuki Kanai, MD, The Division of Internal Medicine, Toyonaka Municipal Hospital, 2-1-1 Okakaminocho, Toyonaka City, Osaka 560, Japan.


*    Abstract
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*Abstract
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Abstract We investigated the relationship between changes in blood pressure and fat distribution after a 12-week low-calorie diet in 26 obese hypertensive women whose average age was 50±13 years, mean body mass index was 33.7±3.1 kg/m2, and mean blood pressure was 112±9 mm Hg. As an index of intra-abdominal fat accumulation, we used the ratio of the intra-abdominal visceral fat area to subcutaneous fat area, determined by a computed tomographic section at the level of the umbilicus. Subjects lost a mean of 9.4±4.1 kg on a 1200-kcal (5040-kJ) diet for 12 weeks. Their mean blood pressure fell from 112±9 to 101±12 mm Hg (P<.001). The ratio of the visceral to subcutaneous fat area was significantly reduced after weight reduction from 0.56±0.33 to 0.45±0.27 (P<.02). Fasting plasma glucose and plasma glucose area after a 75-g oral glucose tolerance test also were significantly reduced by weight reduction. The change in mean blood pressure after weight reduction was not correlated with the change in body weight or body mass index but was correlated with the reduction in visceral fat area or ratio of visceral fat to subcutaneous fat area. Changes in mean blood pressure also were correlated with changes in fasting plasma glucose levels and the plasma glucose area determined by 75-g oral glucose tolerance test. Results indicate that a decrease in intra-abdominal visceral fat, rather than simply of body weight, may reduce blood pressure in obese hypertensive subjects. The mechanism may involve an improvement in glucose tolerance caused by weight reduction.


Key Words: obesity • hypertension • weight reduction • visceral fat


*    Introduction
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*Introduction
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Body weight and blood pressure (BP) have been consistently correlated in several populations.1 2 3 4 5 6 7 8 9 10 11 12 13 14 Short-term weight loss has been shown to substantially reduce BP.15 16 17 18 19 20 21 22 23 24 25 26 27 During the first 2 weeks of a low-calorie diet, there was rapid weight loss and marked natriuresis, together with a significant decrease in BP. A more gradual fall in BP was noted thereafter.17 It is not known why such weight reduction reduces the BP of obese hypertensive subjects and which factors may be most important in this BP fall.

In 1983, we developed a method for estimating fat distribution by means of a computed tomographic (CT) scan.28 We found that the accumulation of intra-abdominal visceral fat is associated with disorders associated with obesity, such as cardiac dysfunction, hypertension, glucose intolerance, and hyperlipidemia. The ratio of the intra-abdominal visceral fat area to the subcutaneous fat area (V/S ratio) at the level of the umbilicus was shown to be a useful and available indication of intra-abdominal visceral fat accumulation.29 30 31 32 33 34 In the present study we investigated the changes in visceral fat accumulation and BP after a 12-week low-calorie diet in obese hypertensive women.


*    Methods
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*Methods
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We evaluated 26 obese hypertensive Japanese women aged 50±13 years (range, 31 to 73) who came to our clinic at The Second Department of Internal Medicine at the Osaka University Hospital for assistance in weight reduction. Men were excluded from study to eliminate the effects of sexual differences.27 35 36 Obese subjects whose body mass index (BMI) was more than 30 kg/m2 were considered for participation. The mean BMI was 33.7±3.1 kg/m2 (30.0 to 38.9). Subjects with systolic BP of 140 mm Hg or higher and/or diastolic BP of 90 mm Hg or higher were defined as hypertensive. All subjects were essential hypertensive individuals with no other circulatory complications. None had received antihypertensive agents. Their body weight had been stable for at least 4 weeks before they consulted our clinic. All subjects gave their informed consent for participation in the study.

Protocol
The subjects' histories were taken at the initial clinic visit. A physical examination was conducted, and laboratory tests were performed. Subjects were instructed to follow a diet that consisted of 1200 kcal/d given as 150 g of carbohydrate, 60 g of protein, 40 g of fat, and 120 mmol of sodium. They were advised to walk for about an hour each day if possible. None of them engaged in a program of vigorous physical exercise. Changes in BP, body weight, topographic parameters, and hormonal and metabolic characteristics in plasma and 24-hour urinary sodium excretion were determined before and after 12 weeks of the low-calorie diet. BP measurements were taken from the right arm with a mercury manometer after the subject had briefly rested in a sitting position. Cuff size was based on girth and length of the upper arm.37 38 Diastolic BP was recorded when the Korotkoff sounds disappeared (phase V). The mean of three BP measurements was used for analysis. Mean BP was calculated as two thirds diastolic BP plus one third systolic BP. Anthropometric measurements included manual measurements of height to the nearest 0.1 cm and weight to the nearest 0.1 kg. The circumferences of the waist and hips were measured to the nearest 0.1 cm at the level of the umbilicus and the widest circumference over the great trochanters, respectively, and were used for calculation of the waist-to-hip circumference ratio. The distribution of body fat was determined by CT scan according to the procedure of Tokunaga et al,28 by which the total cross-sectional area, subcutaneous fat area, and intra-abdominal visceral fat area were measured at the level of the umbilicus. All CT scans were performed with the subjects supine with the use of a CT/T scanner (General Electric Co), and the V/S ratio was calculated. The V/S ratio was adopted as an index of the relative increase in visceral fat, as previously reported by our group.29 30 31 32 33 34 The V/S ratio at the level of the fourth lumbar vertebra or iliac crests is adopted by some investigators35 39 40 41 ; however, such levels are close to the umbilicus in most patients. Blood was drawn after an overnight fast. The blood samples for plasma renin activity, aldosterone, epinephrine, and norepinephrine assays were collected in cold tubes containing disodium EDTA (1.5 mg/mL) and stored at -80°C. Plasma renin activity and aldosterone concentration were determined by radioimmunoassay. Plasma epinephrine and norepinephrine were assayed by high-performance liquid chromatography. A 75-g oral glucose tolerance test also was performed. Blood samples were collected at 0, 30, 60, 90, 120, and 180 minutes for determination of plasma glucose and insulin levels. Plasma glucose was assayed by a glucose oxidase method, and plasma insulin was assayed by double-antibody radioimmunoassay. The plasma glucose area and insulin area were determined by calculating the area under the concentration curve, ie, by multiplying the 30 minutes by the sum of one half the fasting level; the levels at 30, 60, 90, and 180 minutes; and 1.5 times the level at 120 minutes. Urinary sodium excretion was also estimated by urine volume for 24 hours. Sodium concentration was measured by the ion electrode method.

Statistics
Results are expressed as mean±SD. The significance of differences between the means of two groups was determined by a paired t test. Linear regression analysis was used to study the relationship between the variances. A level of P<.05 was accepted as statistically significant.


*    Results
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*Results
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Before the study was started, we observed that the relationships between the V/S ratio and systolic (r=.58, P<.01), diastolic (r=.41, P<.05), or mean (r=.54, P<.01) BP were significantly correlated, as shown in Fig 1Down. Changes in anthropometric parameters after the 12-week 1200-kcal diet are shown in Table 1Down. The subjects lost a mean of 9.4±4.1 (range, 5.5 to 16.0) kg. The weight loss was unexpectedly small in some subjects because of their failure to adhere to the diet. As expected, systolic and diastolic BPs were significantly reduced by weight reduction. The waist circumference, hip circumference, and waist-to-hip ratio were all reduced slightly but significantly. The visceral fat area, subcutaneous fat area, and V/S ratio at the level of the umbilicus were also significantly reduced. Changes in plasma hormonal levels, glucose metabolism, and sodium excretion are shown in Table 2Down. Plasma aldosterone and norepinephrine levels were significantly reduced after weight reduction. Fasting plasma glucose levels, insulin levels, and plasma glucose area were also significantly reduced. There were no significant changes in plasma renin activity, epinephrine, and mean plasma insulin area, although they were markedly decreased in some cases. Sodium excretion was also significantly reduced after weight reduction.



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Figure 1. Scatterplots show correlation between the ratio of visceral fat to subcutaneous fat area (V/S) and blood pressure (BP) at baseline.


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Table 1. Changes in Blood Pressure and Anthropometric Parameters After a 12-Week Low-Calorie Diet in Hypertensive Obese Subjects


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Table 2. Changes in Plasma Hormone Levels and Glucose Metabolism After a 75-g Oral Glucose Tolerance Test and 12-Week Low-Calorie Diet in Hypertensive Obese Subjects

The relationships between the change in mean BP and some parameters that were significantly changed after weight reduction are shown in Table 3Down. Changes in BP are represented by the mean BP for simplicity. The changes in both visceral fat area and V/S ratio were significantly correlated with changes in mean BP. However, the changes in weight, BMI, waist-to-hip ratio, and subcutaneous fat area were not correlated with the changes in mean BP. The changes in the V/S ratio were not correlated with the changes in body weight (r=.22, P=NS), BMI (r=.31, P=NS), and waist-to-hip ratio (r=.10, P=NS). The changes in fasting plasma glucose and plasma glucose area were also significantly correlated with the changes in mean BP. Any other changes in endocrinologic and metabolic characteristics evaluated in this study were not correlated. A scatterplot between the changes in V/S ratio and mean BP that showed the most significant correlation in Table 3Down is depicted in Fig 2Down. Finally, the CT scans at the level of the umbilicus of two representative subjects are shown in Fig 3Down. The subjects of case 1 and case 2 lost 10.0 and 12.0 kg during the study, respectively. Interestingly, the V/S ratio in case 1 was lowered considerably, and that in case 2 was unaltered even after weight reduction. Furthermore, a significant fall in BP was observed only in case 1.


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Table 3. Correlation Coefficient Between Changes in Each Factor and Mean Blood Pressure



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Figure 2. Scatterplot shows correlation between changes in the ratio of visceral fat to subcutaneous fat area (V/S) and mean blood pressure (BP) after weight reduction.



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Figure 3. Computed tomographic scans at the level of the umbilicus of two representative cases. The subject of case 1 is a 36-year-old woman, with height of 154 cm; her weight decreased from 77.5 to 67.5 kg, her ratio of visceral fat to subcutaneous fat area (V/S) decreased from 0.85 to 0.24, and her mean blood pressure decreased from 149 to 116 mm Hg. The subject of case 2 is a 68-year-old woman, with height of 162 cm; her weight decreased from 98.0 to 86.0 kg, her V/S ratio slightly increased from 0.57 to 0.58, and her mean blood pressure changed from 119 to 118 mm Hg after a 12-week low calorie diet. R indicates right; L, left.


*    Discussion
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up arrowIntroduction
up arrowMethods
up arrowResults
*Discussion
down arrowReferences
 
In the present study, which dealt with severely obese subjects, we found that the V/S ratio and systolic, diastolic, or mean BP were closely correlated before the study was started. This result was consistent with our previous report.34 Moreover, changes in the V/S ratio were closely correlated with changes in BP rather than with those in body weight or other topographic parameters. These data suggest that an increase in visceral fat relative to subcutaneous fat may be involved in the pathogenesis of hypertension in obese subjects. Concerning the changes in endocrinologic or metabolic factors in our study, many such factors were significantly reduced by weight reduction, as has been previously reported.15 16 17 18 19 20 21 22 23 24 25 26 27 However, the changes in fasting plasma glucose and plasma glucose area after a 75-g oral glucose tolerance test were significantly correlated with the changes in mean BP. The changes in V/S ratio were also correlated with the changes in fasting plasma glucose (r=.42, P<.05) and plasma glucose area (r=.51, P<.01) (data not shown). These findings indicate that a relative decrease in visceral fat may be involved in the reduction of BP via an improvement in glucose tolerance.6 8 9 10 11 13 24 42 Generally speaking, an improvement in glucose tolerance must reflect a lessening of insulin resistance. Accordingly, insulin resistance may be important in the pathogenesis of hypertension in obese subjects,43 44 as reported for patients with essential hypertension.45

Why didn't insulin secretion fall significantly after weight reduction in our study? Obese Japanese subjects do not necessarily have hyperinsulinemia even though they have severe insulin resistance, even if they do not have diabetes mellitus. Insulin secretion is thought to be exhausted in such cases. Fortunately, however, most of the subjects recovered insulin secretion by weight reduction. Consequently, insulin levels in our study didn't show a significant fall by weight reduction. Exactly which factor promoted the decrease in visceral fat and why the change in visceral fat differed among the subjects studied remain to be determined. Factors such as sexual hormones, aging, heredity, dietary content, daily amount of exercise, and other factors may be involved.46 47 Although the dietary content and daily amount of exercise were quite consistent in the present study, the change in V/S ratio varied among subjects. Further investigations are required to clarify the mechanism.

In conclusion, a loss of intra-abdominal visceral fat may induce a fall of BP in obese hypertensive subjects. The mechanism may involve an improvement in glucose intolerance brought about by weight reduction.

Received April 26, 1995; first decision July 24, 1995; accepted August 31, 1995.


*    References
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up arrowAbstract
up arrowIntroduction
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up arrowResults
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*References
 
1. Whyte HM. Blood pressure and obesity. Circulation. 1956;19:511-516.

2. Alexander JK. Obesity and cardiac performance. Am J Cardiol. 1964;14:860-865. [Medline] [Order article via Infotrieve]

3. Kannel WB, Brand N, Skinner JJ Jr, Dawber TR, McNamara PM. The relation of adiposity to blood pressure and development of hypertension: The Framingham Study. Ann Intern Med. 1967;67:48-59.

4. Stamler R, Stamler J, Riedlinger WF, Algera G, Roberts RH. Weight and blood pressure: findings in hypertension screening of 1 million Americans. JAMA. 1978;240:1607-1610. [Abstract/Free Full Text]

5. Bray GA. Complications of obesity. Ann Intern Med. 1985;103:1052-1063.

6. Christlieb AR, Krolewski AS, Warram JH, Soeldner JS. Is insulin the link between hypertension and obesity? Hypertension. 1985;7(suppl II):II-54-II-57.

7. Frohlich ED, Messerli FH, Reisin E, Dunn FG. The problem of obesity and hypertension. Hypertension. 1985;5(suppl III):III-71-III-78.

8. Modan M, Halkin H, Almog S, Lusky A, Eshkol A, Shefi M, Shitrit A, Fuchs Z. Hyperinsulinemia: a link between hypertension obesity and glucose intolerance. J Clin Invest. 1985;75:809-815.

9. Lucas CP, Estigarribia JA, Darga LL, Reaven GM. Insulin and blood pressure in obesity. Hypertension. 1985;7:702-706. [Abstract/Free Full Text]

10. Manicardi V, Camellini L, Bellodi G, Coscelli C, Ferrannini E. Evidence for an association of high blood pressure and hyperinsulinemia in obese man. J Clin Endocrinol Metab. 1986;62:1302-1304. [Free Full Text]

11. Weinsier RL, Norris DJ, Birch R, Bernstein RS, Pi-Sunyer FX, Yang M, Wang J, Pierson RN Jr, Van Itallie TB. Serum insulin and blood pressure in an obese population. Int J Obes. 1986;10:11-17. [Medline] [Order article via Infotrieve]

12. MacMahon S, Cutler J, Brittain E, Higgins M. Obesity and hypertension: epidemiological and clinical issues. Eur Heart J. 1987;8(suppl B):57-70.

13. Kanai H, Matsuzawa Y, Tokunaga K, Keno Y, Kobatake T, Fujioka S, Nakajima T, Tarui S. Hypertension in obese children: fasting insulin levels are closely correlated with blood pressure. Int J Obes. 1990;14:1047-1056.[Medline] [Order article via Infotrieve]

14. Spiegelman D, Israel RG, Bouchard C, Willett WC. Absolute fat mass, percent body fat, and body-fat distribution: which is the real determinant of blood pressure and serum glucose? Am J Clin Nutr. 1992;55:1033-1044. [Abstract/Free Full Text]

15. Dahl LK, Silver L, Christie RW. The role of salt in the fall of blood pressure accompanying reduction in obesity. N Engl J Med. 1958;258:1186-1192.

16. Ramsay LE, Hettiarachchi J, Davies DL, Winchester J. Weight reduction in a blood pressure clinic. Br Med J. 1978;2:244-245.

17. Tuck ML, Sowers J, Dornfeld L, Kledzik G, Maxwell M. The effect of weight reduction on blood pressure, plasma renin activity, and plasma aldosterone levels in obese patients. N Engl J Med. 1981;304:930-933. [Abstract]

18. Stokholm KH, Nielsen PE, Quaade F, members of the Danish Obesity Project. Correlation between initial blood pressure and blood pressure decrease after weight loss. Int J Obes. 1982;6:307-312. [Medline] [Order article via Infotrieve]

19. Berchtold P, Jörgens V, Kemmer FW, Berger M. Obesity and hypertension: cardiovascular response to weight reduction. Hypertension. 1982;4(suppl III):III-50-III-55.

20. Reisin E, Frohlich ED. Effect of weight reduction on arterial pressure. J Chronic Dis. 1982;35:887-891. [Medline] [Order article via Infotrieve]

21. Reisin E, Frohlich ED, Messerli FH, Dreslinski GR, Dunn FG, Jones MM, Batson HM Jr. Cardiovascular changes after weight reduction in obesity hypertension. Ann Intern Med. 1983;98:315-319.

22. Fagerberg B, Andersson O, Nilsson U, Hedner T, Isaksson B, Björntorp P. Weight-reducing diet: role of carbohydrates on sympathetic nervous activity and hypotensive response. Int J Obes. 1984;8:237-243. [Medline] [Order article via Infotrieve]

23. Andersson OK, Fagerberg B, Hedner T. Importance of dietary salt in the hemodynamic adjustment to weight reduction in obese hypertensive men. Hypertension. 1984;6:814-819. [Abstract/Free Full Text]

24. Rocchini AP, Katch V, Schork A, Kelch RP. Insulin and blood pressure during weight loss in obese adolescents. Hypertension. 1987;10:267-273. [Abstract/Free Full Text]

25. Novi RF, Porta M, Lamberto M, Molinatti GM. Reductions of body weight and blood pressure in obese hypertensive patients treated by diet: a retrospective study. Pan Minerva Med. 1989;31:13-15.

26. Rocchini AP, Key J, Bondie D, Chico R, Moorehead C, Katch V, Martin M. The effect of weight loss on the sensitivity of blood pressure to sodium in obese adolescents. N Engl J Med. 1989;321:580-585. [Abstract]

27. Kotchen JM, Cox-Ganser J, Wright CJ, Kotchen TA. Gender differences in obesity related cardiovascular disease risk factors among participants in a weight loss programme. Int J Obes. 1993;17:145-151.

28. Tokunaga K, Matsuzawa Y, Ishikawa K, Tarui S. A novel technique for determination of body fat by computed tomography. Int J Obes. 1983;7:437-445. [Medline] [Order article via Infotrieve]

29. Fujioka S, Matsuzawa Y, Tokunaga K, Tarui S. Contribution of intra-abdominal fat accumulation to the impairment of glucose and lipid metabolism in human obesity. Metabolism. 1987;36:54-59. [Medline] [Order article via Infotrieve]

30. Tarui S, Fujioka S, Tokunaga K, Matsuzawa Y. Comparison of pathophysiology between subcutaneous-type and visceral-type obesity. In: Bray GA, LeBlanc J, Inoue S, Suzuki M, eds. Diet and Obesity. Tokyo, Japan: Japan Scientific Society Press; 1988:143-152.

31. Fujioka S, Matsuzawa Y, Tokunaga K, Kawamoto T, Kobatake T, Keno Y, Tarui S. Comparison of a novel classification of obesity (visceral fat obesity and subcutaneous fat obesity) with previous classifications of obesity concerning body features or adipose tissue cellularity. In: Björntorp P, Rössner S, eds. Obesity in Europe 88. London, UK: John Libbey; 1988:85-89.

32. Nakajima T, Fujioka S, Tokunaga K, Matsuzawa Y, Tarui S. Correlation of intraabdominal fat accumulation and left ventricular performance in obesity. Am J Cardiol. 1989;64:369-373. [Medline] [Order article via Infotrieve]

33. Matsuzawa Y, Fujioka S, Tokunaga K, Tarui S. Classification of obesity with respect to morbidity. Asian Med J. 1989;32:435-441.

34. Kanai H, Matsuzawa Y, Kotani K, Keno Y, Kobatake T, Nagai Y, Fujioka S, Tokunaga K, Tarui S. Close correlation of intra-abdominal fat accumulation to hypertension in obese women. Hypertension. 1990;16:484-490. [Abstract/Free Full Text]

35. Dixson AK. Abdominal fat assessed by computed tomography: sex difference in distribution. Clin Radiol. 1983;34:189-191. [Medline] [Order article via Infotrieve]

36. Kotani K, Tokunaga K, Fujioka S, Kobatake T, Keno Y, Yoshida S, Shimomura I, Tarui S, Matsuzawa Y. Sexual dimorphism of age related changes in whole-body fat distribution in the obese. Int J Obes. 1994;18:207-212. [Medline] [Order article via Infotrieve]

37. Karvonen MJ, Telivuo LJ, Järvinen EJK. Sphygmomanometer cuff size and the accuracy of indirect measurement of blood pressure. Am J Cardiol. 1964;13:688-693. [Medline] [Order article via Infotrieve]

38. Forsberg SA, DeGuzman M, Berlind S. Validity of blood pressure measurement with cuff in the arm and forearm. Acta Med Scand. 1970;188:389-396. [Medline] [Order article via Infotrieve]

39. Ashwell M, Cole TJ, Dixon AK. Obesity: new insight into the anthropometric classification of fat distribution shown by computed tomography. Br Med J. 1985;290:1692-1694.

40. Sjöström L, Kvist H, Cederblad Å, Tylén U. Determination of total adipose tissue and body fat in women by computed tomography, 40K, and tritium. Am J Physiol. 1986;250:E736-E745. [Abstract/Free Full Text]

41. Peiris A, Sothmann MS, Hoffmann RG, Hennes MI, Wilson CR, Gustafson AB, Kissebah AH. Adiposity, fat distribution, and cardiovascular risk. Ann Intern Med. 1989;110:867-872.

42. Muller DC, Elahi D, Pratley RE, Tobin JD, Andres R. An epidemiological test of hyperinsulinemia-hypertension hypothesis. J Clin Endocrinol Metab. 1993;76:544-548. [Abstract]

43. Reaven GM. Role of insulin resistance in human disease. Diabetes. 1988;37:1595-1607. [Abstract]

44. Vague P, Raccar D. The syndrome of insulin resistance. Horm Res. 1992;38:28-32.

45. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Oleggini M, Graziadei L, Pedrinelli R, Brandi L, Bevilacqua S. Insulin resistance in essential hypertension. N Engl J Med. 1987;317:350-357. [Abstract]

46. Keno Y, Matsuzawa Y, Tokunaga K, Fujioka S, Kawamoto T, Kobatake T, Tarui S. High sucrose diet increases visceral fat accumulation in VMH-lesioned obese rat. Int J Obes. 1991;15:205-211. [Medline] [Order article via Infotrieve]

47. Shimomura I, Tokunaga K, Kotani K, Keno Y, Yanase-Fujiwara M, Kanosue K, Jiao S, Funahashi T, Kobatake T, Yamamoto T, Matsuzawa Y. Marked reduction of acyl-CoA synthetase activity and mRNA in intra-abdominal visceral fat by physical exercise. Am J Physiol. 1993;265:E44-E50.[Abstract/Free Full Text]




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