Regional differences in the control of lipolysis in human adipose tissue

Östman, Jan; Arner, Peter; Engfeldt, Peter; Kager, L

doi:10.1016/0026-0495(79)90131-8

Cited by 262 publications

(142 citation statements)

References 18 publications

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“…27 It has been suggested that the resulting free fatty acid release into the hepatic portal system results in insulin resistance. These metabolic differences between the adipocytes in the various fat depots have been used to explain previous ®ndings that intraabdominal fat mass was a major determinant of insulin resistance.…”

Section: Discussionmentioning

confidence: 99%

Body fat distribution and cardiovascular risk in normal weight women. Associations with insulin resistance, lipids and plasma leptin

Tai

Lau

et al. 2000

Int J Obes

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OBJECTIVE: To systematically examine the correlations between insulin resistance, plasma leptin concentration, obesity and the distribution of fat assessed by anthropometry and magnetic resonance imaging in Asian women. DESIGN: A cross sectional study of non-diabetic, normal weight women. SUBJECTS: Twenty-one healthy women aged 38.8 y (s.d. 11.7) and BMI 22.6 kgam 2 (s.d. 2.3). MEASUREMENTS: Intraperitoneal, retroperitoneal and subcutaneous abdominal fat volume was assessed by magnetic resonance imaging. Anthropometric data were collected. Total fat mass was assessed by bioelectric impedance analysis. Fasting serum lipids, insulin and plasma leptin were assayed. RESULTS: Generalized obesity correlated with subcutaneous abdominal fat mass (r 0.83, P`0.001), but not with intra-abdominal fat mass. Both intraperitoneal fat mass and retroperitoneal fat mass increased with age (r 0.58, P 0.005 and r 0.612, P 0.003, respectively). Abdominal subcutaneous fat mass was the most important determinant of insulin resistance and plasma leptin. Of the serum lipids, only fasting triglyceride correlated signi®cantly with the waist-to-hip ratio. CONCLUSIONS: It is possible that the large size of the subcutaneous depot compared to the intra-abdominal depot overwhelms any metabolic differences between adipose tissue from these two sites, resulting in the stronger correlation between insulin resistance and subcutaneous abdominal fat mass rather than intra-abdominal fat mass. On the other hand, the distribution of fat between subcutaneous fat depots may be important in the metabolic syndrome given the correlation of fasting triglyceride with waist to hip ratio but not with abdominal fat. However, the study population was small, younger and leaner compared to previous studies and we may not be able to generalize these results to all segments of the population. We con®rm that subcutaneous fat mass is the major determinant of plasma leptin.

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Section: Discussionmentioning

confidence: 99%

Body fat distribution and cardiovascular risk in normal weight women. Associations with insulin resistance, lipids and plasma leptin

Tai

Lau

et al. 2000

Int J Obes

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“…These show that although smaller babies have reduced subcutaneous fat with the reduction proportionate to birth size, visceral fat is preserved so that the smaller babies have relative visceral adiposity. 24,25 Given the labile function of visceral fat, 35 this provides a plausible route to later metabolic compromise.…”

Section: The 'Mismatch' or 'Thrifty' Pathwaymentioning

confidence: 99%

Developmental and epigenetic pathways to obesity: an evolutionary-developmental perspective

2008

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Although variation in individual lifestyle and genotype are important factors in explaining individual variation in the risk of developing obesity in an obesogenic environment, there is growing evidence that developmentally plastic processes also contribute. These effects are mediated at least in part through epigenetic processes. These developmental pathways do not directly cause obesity but rather alter the risk of an individual developing obesity later in life. At least two classes of developmental pathway are involved. The mismatch pathway involves the evolved adaptive responses of the developing organism to anticipated future adverse environments, which have maladaptive consequences if the environment is mismatched to that predicted. This pathway can be cued by prenatal undernutrition or stresses that lead the organism to forecast an adverse future environment and change its developmental trajectory accordingly. As a result, individuals develop with central and peripheral changes that increase their sensitivity to an obesogenic environment. It provides a model for how obesity emerges in populations in rapid transition, but also operates in developed countries. There is growing experimental evidence that this pathway can be manipulated by, for example, postnatal leptin exposure. Secondly, maternal diabetes, maternal obesity and infant overfeeding are associated with a greater risk of later obesity. Early life offers a potential point for preventative intervention.

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“…It is possible that the intra-abdominal fat depots, although relatively small in comparison with subcutaneous depots, play an important role in normal buffering. Rates of lipolysis from intra-abdominal adipocytes, when measured in vitro, tend to be high [78,79,80], and these high rates of lipolysis must be matched in the postprandial period by high rates of fat deposition [81]. There is some direct evidence for the latter in vivo [82].…”

Section: Site-specific Properties Of Adipose Tissuementioning

confidence: 99%