Effects of body fat distribution on regional lipolysis in obesity.

Martin, Mary Lane; Jensen, Michael D.

doi:10.1172/jci115345

Cited by 246 publications

(189 citation statements)

References 32 publications

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“…In premenopausal obese women with similar BMI, whole-body NEFA release was higher in subjects with a high compared to low waist to hip circumference ratio (WHR), as could be expected. 23 Interestingly, however, this was not only due to a smaller NEFA release from the lower-body fat but also Lower-body fat and insulin sensitivity B Buemann et al attributable to the fact that the women with a low WHR released less NEFA from their upper body fat depots per kilogram fat mass. In line with these findings, both subcutaneous abdominal and gluteal adipocytes from upper body obese white women have been reported to be less sensitive to insulin, both with regard to the effect on lipolysis and on glucose uptake, compared to adipocytes achieved from the same sites in lower-body obese white women.…”

Section: Discussionmentioning

confidence: 99%

Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin

et al. 2005

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AIMS:To study the association between lower-body fat and estimates of whole-body insulin sensitivity in middle-aged men with and without a history of juvenile onset obesity, and to determine the possible mediating role of fasting serum adiponectin level as an insulin-sensitizing peptide. METHODS: A total of 401 men aged 39-65 y, body mass index 18-54 kg/m 2 , participated in the study. The following variables were measured on the study participants: regional body fat distribution as assessed by dual energy X-ray absorptiometry, abdominal sagittal diameter, maximal oxygen uptake (VO 2 max), physical activity, fasting and post-glucose load levels of plasma glucose, serum insulin, and blood non-esterified fatty acid plus fasting levels of serum adiponectin and HbA1c. RESULTS: Lower-body fat mass was positively associated with insulin sensitivity as estimated by Matsudas index also after adjusting for age, lean tissue mass, trunkal fat mass, weight changes since draft board examination, VO 2 max and the level of physical activity. In a subgroup of men selected for a large lower-body fat mass, fasting serum insulin concentration was 24% lower (Po0.01) and fasting serum adiponectin 33% higher (Po0.005) compared to a subgroup of men with a small lower-body fat mass but with similar trunkal fat mass. CONCLUSION: Lower-body fat mass is positively associated with an estimate of insulin sensitivity independently of trunkal fat mass in both lean and obese middle-aged men and this effect could partly be statistically explained by variations in serum adiponectin levels.

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Section: Discussionmentioning

confidence: 99%

Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin

et al. 2005

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“…Upper-body fat is the major contributor of systemic nonesterified fatty acids, hence showing a higher lipolysis rate when compared with the lower-body fat depot. 42,43 The rate of action of the enzyme hormone-sensitive lipase, a key enzyme in lipolysis, is lower in the gluteal than the abdominal depot. 44 Starvation for 72 h results in increased lipolysis in the abdominal depot but not in gluteofemoral fat.…”

Section: Fatty Acid Storage and Releasementioning

confidence: 99%

Gluteofemoral body fat as a determinant of metabolic health

2010

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Body fat distribution is an important metabolic and cardiovascular risk factor, because the proportion of abdominal to gluteofemoral body fat correlates with obesity-associated diseases and mortality. Here, we review the evidence and possible mechanisms that support a specific protective role of gluteofemoral body fat. Population studies show that an increased gluteofemoral fat mass is independently associated with a protective lipid and glucose profile, as well as a decrease in cardiovascular and metabolic risk. Studies of adipose tissue physiology in vitro and in vivo confirm distinct properties of the gluteofemoral fat depot with regards to lipolysis and fatty acid uptake: in day-to-day metabolism it appears to be more passive than the abdominal depot and it exerts its protective properties by long-term fatty acid storage. Further, a beneficial adipokine profile is associated with gluteofemoral fat. Leptin and adiponectin levels are positively associated with gluteofemoral fat while the level of inflammatory cytokines is negatively associated. Finally, loss of gluteofemoral fat, as observed in Cushing's syndrome and lipodystrophy is associated with an increased metabolic and cardiovascular risk. This underlines gluteofemoral fat's role as a determinant of health by the long-term entrapment of excess fatty acids, thus protecting from the adverse effects associated with ectopic fat deposition.

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“…Systolic BP (SBP) increased in both groups, but the increase was significantly greater in subjects with positive than those with no family history of hypertension (1472 vs 1072 mm Hg). 26 Based on such data, it can be speculated that in subjects that typically exhibit chronic NEFA elevation, that is those with central obesity, IR and type II diabetes, [4][5][6] this NEFA increase can be an important factor promoting the development of hypertension in subjects with normal BP levels, or deteriorating BP control in patients with already elevated BP. Further, some of the above data 21,22 support not only a close association between NEFA and BP, but also that this relation could be independent from the degree of IR and other parameters of the metabolic syndrome.…”

Section: The Effect Of Nefas On Bp Levelsmentioning

confidence: 99%

“…4 One of the most important factors connecting obesity with the development of related metabolic abnormalities is the elevated release of free or non-esterified fatty acids (NEFAs) from abdominal adipocytes in patients with central obesity, which results in increase in plasma NEFA concentration and turnover. 5,6 NEFAs have been shown to induce both hepatic and peripheral IR, 7,8 to activate apoptotic pathways in pancreatic b cells, 9 to promote endothelial dysfunction 10 and to increase the production of plasminogen activator inhibitor-1. 11 Most importantly, increased NEFA supply of the liver, primarily owing to the incomplete insulin-mediated suppression of lipolysis in this type of subjects, is the initial step for the development of the characteristic lipid disorders of the metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension in subjects with obesity/insulin resistance?

Sarafidis

Bakris

2006

J Hum Hypertens

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The prevalence of hypertension in individuals with obesity or type II diabetes is substantially elevated. Increased levels of non-esterified fatty acids (NEFAs) in abdominally obese subjects were reported to contribute in the development of various disturbances related to the metabolic syndrome, such as hepatic and peripheral insulin resistance (IR), dyslipidaemia, b-cell apoptosis, endothelial dysfunction and others. However, the involvement of NEFAs in the development of hypertension has been much less studied in comparison to other mechanisms linking IR and central obesity with blood pressure (BP) elevation. This article reviews the existing evidence on the relation between NEFA and hypertension in an attempt to shed a light on it. In vivo data from both animal and human studies support that acute plasma NEFA elevation leads to increase in BP levels, whereas epidemiological evidence suggests a link between increased NEFA levels and hypertension. Further, accumulating data indicate the existence of several pathways through which NEFAs could promote BP elevation, that is a 1 -adrenergic stimulation, endothelial dysfunction, increase in oxidant stress, stimulation of vascular cell's growth and others. The above data support a possible important role of NEFA in hypertension development in patients with obesity and the metabolic syndrome and raise hypotheses for future research.

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Effects of body fat distribution on regional lipolysis in obesity.

Abstract: To determine the contribution of the major body fat depots to systemic free fatty acid (FFA)

Cited by 246 publications

References 32 publications

Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin

Lower-body fat mass as an independent marker of insulin sensitivity—the role of adiponectin

Gluteofemoral body fat as a determinant of metabolic health

Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension in subjects with obesity/insulin resistance?

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