Gender differences in the relationship between leptin, insulin resistance and the autonomic nervous system

Flanagan, Daniel; Vaile, J.; Petley, Graham W.; Phillips, David I. W.; Godsland, Ian F.; Owens, P. C.; Moore, Vivienne; Cockington, Richard A.; Robinson, Siân

doi:10.1016/j.regpep.2006.11.009

Cited by 53 publications

(50 citation statements)

References 25 publications

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“…In contrast, in the T1-diabetes model we do not observe gender diVerences in bone responses. In humans, serum leptin levels are higher in females compared to males (Flanagan et al 2007;Karaguzel et al 2006;Kiess et al 1998;Thrailkill et al 2001), similar to our Wndings; however, the eVect of diabetes on leptin levels is inconsistent. At the time of diagnosis serum leptin levels are reported to be reduced (Kiess et al 1998), but with insulin treatment and its associated increase in body mass index leptin levels are restored to normal levels (Hernandez et al 2004;Karaguzel et al 2006;Lo et al 2004;Thrailkill et al 2001).…”

Section: Controlsupporting

confidence: 88%

Type I diabetic bone phenotype is location but not gender dependent

Martin

McCabe

2007

Histochem Cell Biol

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Bone is highly dynamic and responsive. Bone location, bone type and gender can influence bone responses (positive, negative or none) and magnitude. Type I diabetes induces bone loss and increased marrow adiposity in the tibia. We tested if this response exhibits gender and location dependency by examining femur, vertebrae and calvaria of male and female, control and diabetic BALB/c mice. Non-diabetic male mice exhibited larger body, muscle, and fat mass, and increased femur BMD compared to female mice, while vertebrae and calvarial bone parameters did not exhibit gender differences. Streptozotocin-induced diabetes caused a reduction in BMD at all sites examined irrespective of gender. Increased marrow adiposity was evident in diabetic femurs and calvaria (endochondrial and intramembranous formed bones, respectively), but not in vertebrae. Leptin-deficient mice also exhibit location dependent bone responses and we found that serum leptin levels were significantly lower in diabetic compared to control mice. However, in contrast to leptin-deficient mice, the vertebrae of T1-diabetic mice exhibit bone loss, not gain. Taken together, our findings indicate that TI-diabetic bone loss in mice is not gender, bone location or bone type dependent, while increased marrow adiposity is location dependent.

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Section: Controlsupporting

confidence: 88%

Type I diabetic bone phenotype is location but not gender dependent

Martin

McCabe

2007

Histochem Cell Biol

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“…This suggests that leptin in women is associated with sympathetic activity. 88 Spontaneous leptin secretion over 24-hour and 48-hour periods shows a genderbased difference that is significantly higher in women than in men. 89 These observations may help to explain the differences in leptin concentrations between men and women.…”

Section: Results From Clinical Surveysmentioning

confidence: 99%

Leptin and Cardiovascular Disease

2008

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L eptin, a 16-kDa hormone identified and cloned in 1994, is synthesized and secreted specifically from white adipose cells. 1 Leptin has a variety of important central and peripheral actions to regulate energy balance and metabolism, fertility, and bone metabolism that are mediated by specific cell surface leptin receptors. 2,3 Importantly, leptin may also exert actions related to cardiovascular homeostasis that are potentially atherogenic, thrombotic, and angiogenic. 4 -6 Leptin has peripheral actions to stimulate vascular inflammation, oxidative stress, and vascular smooth muscle hypertrophy that may contribute to pathogenesis of type 2 diabetes mellitus, hypertension, atherosclerosis, and coronary heart disease. 3,4,7 Insulin resistance, 8 systemic hypertension, and hypercholesterolemia 9 all contribute independently to vascular endothelial dysfunction that promotes atherosclerosis and coronary heart disease. Reciprocal relationships between endothelial dysfunction and insulin resistance are characterized by impaired insulin-stimulated nitric oxide (NO) production from endothelium that decreases blood flow to insulin target tissues. 10,11 Relationships among obesity, metabolic syndrome, diabetes mellitus, and their cardiovascular complications are well established. However, the mechanisms by which excess adiposity causes both insulin resistance and vascular dysfunction are not well understood. Direct vascular effects of adipokines such as leptin are attractive candidates that may help to explain underlying pathophysiological mechanisms.Several clinical studies demonstrate that hyperleptinemia predicts acute cardiovascular events, restenosis after coronary injury such as angioplasty, and cerebral stroke independent of traditional risk factors. 12-14 Leptin-deficient hyperlipidemic mice (ob/ob; apolipoprotein E [apoE] Ϫ/Ϫ mice) develop significantly less atherosclerosis than apoE Ϫ/Ϫ mice on an atherogenic diet. Exogenous leptin significantly increases atherosclerotic areas in apoE Ϫ/Ϫ mice. Taken together, these findings support the notion that leptin accelerates atherosclerosis. 15 By contrast, some data indicate that leptin may protect against atherosclerosis in specific animal models. For example, low-density lipoprotein-receptor knockout mice lacking leptin (LDLR Ϫ/Ϫ ob/ob) develop more atherosclerotic lesions than LDLR Ϫ/Ϫ control mice. 16 Moreover, in 207 women with normal glucose tolerance, impaired glucose tolerance, or type 2 diabetes mellitus, low plasma leptin predicted cardiovascular mortality during a 7-year follow-up period. 17 Thus, the net effects of leptin on cardiovascular pathophysiology are complex and not completely understood.In this review, we discuss cardiovascular actions of leptin related to atherosclerosis, insulin resistance, and hypertension. Particular emphasis is given to insights derived from therapeutic interventions with lifestyle modification, cardiovascular drugs, antidiabetic drugs, and other related treatments. Biology and Metabolism of LeptinThe adipocyte is an active ...

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“…Likewise, the lower MMI in females is probably due to their lower serum TC [7] and IS [14,17,34]. In fact, numerous previous studies have constantly reported that TC is significantly positively associated with IS in vivo [24,38,40,46,54], and both of them can be improved with MMIs, muscle mass indexes, were expressed as mean ± SD exercise [3,5,11,20,36,37,42,48].…”

Section: Discussionmentioning

confidence: 97%

The differences of sarcopenia-related phenotypes: effects of gender and population

Zhong

Lei

Yang

et al. 2011

Eur Rev Aging Phys Act

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Sarcopenia is a serious condition especially in the elderly population mainly characterized by the loss of skeletal muscle mass and strength with aging. Extremity skeletal muscle mass index (EMMI) (sum of skeletal muscle mass in arms and legs/height 2 ) is gaining popularity in sarcopenia definition (less than two standard deviations below the mean of a young adult reference group), but little is known about the gender-and population-specific differences of EMMI. This study aimed at investigating the differences of EMMI, arm muscle mass index (AMMI), and leg muscle mass index (LMMI) between gender groups and populations (Chinese vs. Caucasians). The participants included 1,809 Chinese and 362 Caucasians with normal weight aged from 19 to 45 years old. Extremity muscle mass, arm muscle mass, and leg muscle mass were measured by using dual energy x-ray absorptiometry. Independent sample t tests were used to analyze the differences in muscle mass indexes between the studied groups. All the study parameters including EMMIs, AMMIs, and LMMIs were significantly higher (P≤0.0003) in the Caucasian group than in the Chinese group and also higher in the male group than in the female group, and these significant differences (P≤0.0005) remained after adjusting for age by simple regressions. The detected differences of muscle mass indexes between different gender and ethnic groups may provide important implications in their different risk of future sarcopenia.

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Gender differences in the relationship between leptin, insulin resistance and the autonomic nervous system

Cited by 53 publications

References 25 publications

Type I diabetic bone phenotype is location but not gender dependent

Type I diabetic bone phenotype is location but not gender dependent

Leptin and Cardiovascular Disease

The differences of sarcopenia-related phenotypes: effects of gender and population

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