Inositol Phosphoglycans and the Regulation of the Secretion of Leptin: In Vitro Effects on Leptin Release from Adipocytes and the Relationship to Obesity

Kunjara, Sirilaksana; Wang, Dennis Y.; McLean, Patricia; Greenbaum, A. L.; Rademacher, Thomas W.

doi:10.1006/mgme.2000.2988

Cited by 11 publications

(6 citation statements)

References 50 publications

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“…As shown in Table 3, behavioral and pharmacological intervention known to improve insulin sensitivity, such as fasting or caloric restriction (19), weight loss, exercise (20), and treatment with thiazolidinediones (21), all are associated with decreased plasma leptin levels. Furthermore, inositol phosphoglycan A, a second-messenger agonist along the insulin signaling pathway, has been shown to inhibit leptin release from cultured adipocytes (22). In contrast, interventions known to induce insulin resistance, such as overfeeding (23), weight gain, and treatment with glucocorticoids (24,25), estrogens (26), or GH (27) result in elevated leptin levels.…”

Section: Discussionmentioning

confidence: 97%

Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Askari

Tykodi

Liu

et al. 2010

The Journal of Clinical Endocrinology &Amp; Metabolism

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Section: Discussionmentioning

confidence: 97%

Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Askari

Tykodi

Liu

et al. 2010

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…It is well documented that insulin stimulates leptin secretion from incubated adipocytes in vitro and that this effect is counteracted by agents increasing intracellular cAMP levels, including lipolytic hormones and specific inhibitors of phosphodiesterase III (Bray and York 1997;Kunjara et al 2000bKunjara et al , 2008Cammisotto and Bukowiecki 2002;Bjorbaek and Kahn 2004;Zhang et al 2005;Fruhbeck 2006;Szkudelski 2007). Thus, the prevailing adipose tissue content of raised IPG-A and lower cAMP in CR rat adipocytes could be influential in the release of leptin and the significantly raised plasma leptin, the sequela there-from including accelerated oxidation of fatty acids by tissues such as muscle.…”

Section: Discussionmentioning

confidence: 97%

Age-related changes in the response of rat adipocytes to insulin: evidence for a critical role for inositol phosphoglycans and cAMP

et al. 2010

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Adipose tissue plays a pivotal role in ageing and longevity; many studies, both human and animal, have focussed on the effects of food limitation. Here we present a new model based on striking differences between two 'normal' inbred strains of albino Wistar rats the Charles River (CR) and Harlan Olac (HO) that have marked differences in age-related accumulation of fat and insulin-stimulated rates of glucose incorporation into lipid in the epididymal fat pads (EFP). The incorporation [U-(14)C]glucose into lipid by adipocytes showed that the CR group had a twofold higher basal rate of lipogenesis and a greater response to insulin in vitro, exceptionally, adipocytes from CR group maintained the high response to insulin to late adulthood while retaining the lower EFP weight/100 g body weight. Inositol phosphoglycan A-type (IPG-A), a putative insulin second messenger, was 3.5-fold higher and cAMP significantly lower per EFP in the CR versus HO groups. Plasma insulin levels were similar and plasma leptin higher in CR versus HO groups. The anomaly of a higher rate of lipogenesis and response to insulin and lower EFP weight in the CR group is interpreted as the resultant effect of a faster turnover of lipid and stimulating effect of leptin in raising fatty acid oxidation by muscle, potentially key to the lower accumulation of visceral fat. The metabolic profile of the CR strain provides a template that could be central to therapies that may lead to the lowering of both adipose and non-adipocyte lipid accumulation in humans in ageing.

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“…The mechanisms underlying changes in lipid and glucose metabolism during normal pregnancy (especially insulin resistance) and their further exacerbation in pregnancies complicated by GDM are generally unknown. A-IPG seems to have a pivotal role in lipogenesis through a negative control on leptin release from adipocytes [17] , a circulating hormone involved in the deposition or oxidation of fat and associated with complications of pregnancy such as pre-eclampsia and gestational diabetes [23] . Leptin was found to correlate with BMI, insulin resistance and glycaemia in pregnancies complicated by GDM [24] .…”

Section: Discussionmentioning

confidence: 99%

“…In fact, A-IPG was significantly increased in the urine of subjects with type 2 diabetes, whereas P-IPG was essentially the same in the diabetic and the control groups. The increased A-IPG production has an inhibitory effect on leptin release with subsequent impairment of fat oxidation [17] .…”

Section: Introductionmentioning

confidence: 99%

Altered Urinary Release of Inositol Phosphoglycan A-Type in Women with Gestational Diabetes Mellitus

Scioscia¹,

Kunjara

Gumaa

et al. 2007

Gynecol Obstet Invest

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Background/Aims: The mechanisms underlying overgrowth of adipose tissue in fetuses of women with gestational diabetes mellitus (GDM) are generally unknown. Inositol phosphoglycan A-type (A-IPG), a putative second messenger of insulin, was reported to regulate lipogenesis in adipose tissue. IPGs have recently been shown to increase during normal pregnancy, in maternal and fetal compartments. Methods: 48 women with GDM and 23 healthy pregnant women were recruited for this cross-sectional study. Levels of A-IPG were assessed enzymatically in urinary specimens and correlated with clinical parameters. Results: A-IPG urinary release was lower in GDM patients (p < 0.01) and correlated positively with BMI (p < 0.01) and negatively with glycaemic control in the diabetic group (postprandial glycaemia and glycated haemoglobin, p < 0.01) in addition to a nearly significant correlation with birth weight (p = 0.08). Furthermore, a lower A-IPG urinary release was found in diabetic subjects with normal fasting glycaemia compared with those with poor fasting glycaemic control (p < 0.05). Conclusions: An altered A-IPG urinary excretion occurs in GDM with a negative correlation with poor glycaemic control. Our data suggest an interesting potential role of this molecule in maternal metabolic control during pregnancy and, possibly, in fetal growth.

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Inositol Phosphoglycans and the Regulation of the Secretion of Leptin: In Vitro Effects on Leptin Release from Adipocytes and the Relationship to Obesity

Cited by 11 publications

References 50 publications

Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Fasting Plasma Leptin Level Is a Surrogate Measure of Insulin Sensitivity

Age-related changes in the response of rat adipocytes to insulin: evidence for a critical role for inositol phosphoglycans and cAMP

Altered Urinary Release of Inositol Phosphoglycan A-Type in Women with Gestational Diabetes Mellitus

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