Long-term kindled seizures induce alterations in hematopoietic functions: Role of serum leptin

Bhatt, Rekha; Bhatt, Suresh; Rameshwar, Pranela; Siegel, Allan

doi:10.1016/j.eplepsyres.2005.06.002

Cited by 15 publications

(10 citation statements)

References 51 publications

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“…30 In view of the low serum leptin levels well established in AN, 31 the hypothesis of a contribution of hypoleptinemia to the hematological abnormalities of these patients appears attractive. We did not measure leptin in a sufficient number of our patients to search for possible correlations with other parameters.…”

Section: Resultsmentioning

confidence: 98%

Low insulin‐like growth factor I and leukopenia in anorexia nervosa

Polli

Scacchi

Giraldi

et al. 2008

Intl J Eating Disorders

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Section: Resultsmentioning

confidence: 98%

Low insulin‐like growth factor I and leukopenia in anorexia nervosa

Polli

Scacchi

Giraldi

et al. 2008

Intl J Eating Disorders

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“…Although elevated leptin levels are present in obesity, it is likely that the physiological importance of leptin is that low levels indicate a state of starvation [2]. Recent data suggest that leptin may regulate a variety of other physiological processes, such as insulin action [7], hemopoiesis [5], immune function [28], reproduction [40], angiogenesis [26], and bone development and remodeling [19]. However, it is not clear whether leptin is a stimulator or an inhibitor of bone growth in humans.…”

Section: Introductionmentioning

confidence: 99%

No Adaptations in Bone of Leptin-Deficient ob/ob Mice in Response to Loading

Heep¹,

Wedemeyer²,

Xu³

et al. 2008

BIOmaterialien

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Leptin is a peptide hormone produced predominantly by white fat cells [1,47]. The mature protein, encoded by the obesity (ob) gene localized in human and mouse 7 and 6 chromosomes, respectively, is a 16 kDa non-glycosylated protein. Leptin levels in the blood are proportional to adipose tissue mass. Initially discovered as a central regulator of appetite and energy expenditure, leptin levels can be considered as a signal to the body regarding its energy reserves. Although elevated leptin levels are present in obesity, it is likely that the physiological importance of leptin is that low levels indicate a state of starvation [2]. Recent data suggest that leptin may regulate a variety of other physiological processes, such as insulin action [7], hemopoiesis [5], immune function [28], reproduction [40], angiogenesis [26], and bone development and remodeling [19]. However, it is not clear whether leptin is a stimulator or an inhibitor of bone growth in humans. Some investigators noted a positive relationship between serum leptin levels and bone mineral density (BMD). Iwamoto et al. described a weakly correlation of serum leptin level with bone mineral density of pelvis and left leg in the premenopausal women and Odebasi et al. found that there was no correlation between plasma leptin concentrations and BMD values in healthy postmenopausal woman but a weak correlation was observed in postmenopausal woman with osteoporosis [23,35]. Whereas others observed a negative relationship. Blum et al. suggest that for a given body weight, a higher proportion of fat and a higher serum leptin concentration have negative associations with bone mass in premenopausal women [6]. Sato et al. suggest that an increase in serum leptin reduces bone formation and decreases BMD in adult men [42]. Furthermore, no associations between serum leptin levels and BMD have been reported, which further confounds the interpretation of leptin's effect on bone mass. Martini et al. conclude that serum leptin have no direct effect on bone mass and bone turnover in healthy postmenopausal women [32] and Rauch et al. appear that leptin has less influence on the mature than on the growing skeleton [41]. Only a few studies in humans have examined the direct effect of leptin administration on BMD. Ogueh et al. [36] Leptin was found to be involved in regulation of bone development and remodeling. This study was performed to evaluate the effects of biomechanical loading due to body weight in leptin-defient ob/ob mice at the same pubertal stage. No significant difference was found between the two groups for all the parameters (p>0.05) suggesting that the presence of leptin may be an important pre-condition for positive correlation between loading and bone mass. Furthermore, concordance of bone formation was found among appendicular regions, but was not found between the axial and appendicular regions.

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“…Then, a rapid rebound of UAG levels respect to those of AG, related to this mechanism, may explain the partial reduction of UAG and total ghrelin levels after the PTZinduced seizure (Ataie et al, 2011). Moreover, some studies described high serum leptin levels in rats after seizures (Bhatt et al, 2005;Hum et al, 2009), which could directly inhibit ghrelin secretion as shown in other animal models (Kamegai et al, 2004). Another possible explanation about lower AG blood levels, is an increased uptake of AG by brain structures influenced by pathophysiological events to modulate epileptic discharges (Ataie et al, 2011;Banks et al, 2002).…”

Section: Ghrelin and Epilepsy: In Vitro And In Animal Studiesmentioning

confidence: 99%