Effects of Selected Minerals on Leptin Secretion in Streptozotocin-lnduced Hyperglycemic Mice

Chen, Ming-Der; Yang, Vivian; Alexander, P. S.; Lin, Pi-Yao; Song, Yuh-Min

doi:10.1177/153537020122600905

Cited by 11 publications

(9 citation statements)

References 34 publications

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“…Currently, studies show that leptin may enhance or diminish bone architecture, and its affects may be mediated both through a central mechanism as well as a peripheral pathway [20]. Leptin concentrations were significantly lower in diabetic mice compared to controls, consistent with previous studies in STZ-induced diabetic rodents [21]. However, IGF-I therapy failed to alter leptin levels in diabetic mice, suggesting that while leptin deficiency might contribute to skeletal deficits observed in diabetic mice, improvements in bone microarchitecture, bone formation and strength achieved with IGF-I therapy cannot be attributed to changes in leptin.…”

Section: 4 Discussionsupporting

confidence: 81%

Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes

Fowlkes

Nyman

Bunn

et al. 2013

Bone

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Objective Using a streptozotocin (STZ)-induced mouse model of type 1 diabetes (T1D), we have previously demonstrated that long-term diabetes inhibits regenerative bone formation during tibial distraction osteogenesis (DO) and perturbs skeletal integrity by decreasing cortical thickness, bone mineral density and bone’s resistance to fracture. Because long-standing T1D is also associated with a deficiency of insulin-like growth factor I (IGF-I), we examined the effects of systemic IGF-I treatment on skeletal microarchitecture and strength, as well as on bone formation in diabetic mice. Research Design and Methods Streptozotocin-induced diabetic or control mice were treated with recombinant human IGF-I (rhIGF-I, 1.5 mg/kg/day as subcutaneous infusion) or vehicle throughout a 14 day DO procedure. Thereafter, trunk blood was assayed for glucose, insulin, rhIGF-I, mouse IGF-I and leptin. Bone formation in distracted tibiae was quantified. Effects on cortical bone strength and trabecular bone architecture were assessed by µCT analysis and three-point bend testing of contralateral femurs. Results New bone formation during DO was reduced in diabetic mice but significantly improved with rhIGF-I treatment. The contralateral femurs of diabetic mice demonstrated significant reductions in trabecular thickness, yield strength and peak force of cortical bone, which were improved with rhIGF-I treatment. rhIGF-I also reduced intracortical porosity in control mice. However, treatment with rhIGF-I did not normalize serum glucose, or correct concurrent deficiencies of insulin or leptin seen in diabetes. Conclusions These findings demonstrate that despite persistent hyperglycemia, rhIGF-I promoted new bone formation and improved biomechanical properties of bone in a model of T1D, suggesting that it may be useful as a fracture preventative in this disease.

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Section: 4 Discussionsupporting

confidence: 81%

Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes

Fowlkes

Nyman

Bunn

et al. 2013

Bone

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“…[33] This is an interesting result as leptin and leptin receptors are structurally similar to IL-6. [33] In conclusion, it was demonstrated that metabolic defects that arise in mice with hyperglycemia induced by STZ could be restored by supplementation of zinc in physiological doses. Maybe the most important study about the relationship between zinc and leptin is the one by Ott and Shay.…”

Section: Leptin and Zinc Relation In Food Intakementioning

confidence: 94%

“…It was reported that zinc deficiency inhibited leptin secretion from the fatty tissue, whereas supplementation of a physiological dose of zinc increased both leptin levels and glucose intake in mice with hyperglycemia induced by streptozotocin (STZ). [33]…”

Section: Leptin and Zinc Relation In Food Intakementioning

confidence: 99%

Leptin and zinc relation : In regulation of food intake and immunity

Baltacı

Moğulkoç

2012

Indian J Endocr Metab

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Leptin is synthesized and released by the adipose tissue. Leptin, which carries the information about energy reserves of the body to the brain, controls food intake by acting on neuropeptide Y (NPY), which exercises a food-intake-increasing effect through relevant receptors in the hypothalamus. Zinc deficiency is claimed to result in anorexia, weight loss, poor food efficiency, and growth impairment. The fact that obese individuals have low zinc and high leptin levels suggests that there is a relation between zinc and nutrition, and consequently also between zinc and leptin. Leptin deficiency increases the predisposition to infections and this increase is associated with the impairments in the production of cytokines. Zinc has a key role in the sustenance of immune resistance against infections. Dietary zinc deficiency negatively affects CD+4 cells, Th functions, and consequently, cell-mediated immunity by causing a decrease in the production of IL-2, IF-γ, and TNF-α, which are Th1 products. The relation between zinc and the concerned cytokines in particular, and the fact that leptin has a part in the immune responses mediated by these cytokines demonstrate that an interaction among cellular immunity, leptin and zinc is inevitable. An overall evaluation of the information presented above suggests that there are complex relations among food intake, leptin and zinc on one hand and among cellular immunity, leptin and zinc on the other. The aim of the present review was to draw attention to the possible relation between zinc and leptin in dietary regulation and cellular immunity.

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“…Chen et al, [16][17] observed increased leptin at low zinc levels and further zinc supplementation to the experimental animals in the same study stimulated further increase in leptin levels. This implies that zinc may either directly affect leptin gene expression or indirectly cause leptin production.…”

Section: Discussionmentioning

confidence: 62%

Attenuation of Gastrointestinal Tract Propulsion in Rats by Zinc Acetate: Investigation into Serotonergic and Dopaminergic Mechanisms

Akomolafe¹

2014

AJLS

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This study evaluated the influence of orally administered zinc acetate on gastrointestinal tract propulsion of rats. It also evaluated the effects of the salt on faecal output and gastrointestinal transit time in the rats. The effects of zinc acetate on feeding as well as water intake were determined. The dose of zinc acetate which produced the maximal effect was used to investigate the receptors involved in the alteration of gastrointestinal motility by the salts. All the three doses of zinc acetate (50 mg/kg, 80 mg/kg and 110 mg/kg) produced a significant reduction in the number of total faecal pellets produced in eight hours of study (2.67 ± 0.67, 10.75 ± 0.60, 5 ± 0.52) respectively when compared with the control group (15.67 ± 0.52). Also, the three doses of zinc acetate produced a dose-dependent significant reduction in the faecal mass (1.23 ± 0.08g, 0.96 ± 0.07g, 0.59 ± 0.07g) respectively when compared with control group (3.39 ± 0.25g).The total transit time in rats treated with 50 mg/kg of zinc acetate (746.2 ± 5.95 minutes) increased significantly compared to the control group (251.2 ± 5.48 minutes). The three doses of zinc acetate produced a dose-dependent reduction (p < 0.05) in food intake (9.67 ± 0.61, 9.17 ± 0.62 and 5.00 ± 0.39) respectively compared to the control group (18.33 ± 0.67). Pre-treatment with metoclopramide (5HT 3 & D 2 blocker/5HT 4 serotonergic agonist) significantly increased faecal pellet output in zinc acetate treated rats (4.80 ± 0.20) when compared with rats treated with zinc acetate alone (2.67 ± 0.67).The study concluded that zinc acetate reduced gastrointestinal tract propulsion in rats evidenced as increased intestinal transit time of rats and reduced faecal pellet output via stimulation of 5HT 3 and 5HT 4 serotonergic and dopaminergic receptors.

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Effects of Selected Minerals on Leptin Secretion in Streptozotocin-lnduced Hyperglycemic Mice

Cited by 11 publications

References 34 publications

Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes

Osteo-promoting effects of insulin-like growth factor I (IGF-I) in a mouse model of type 1 diabetes

Leptin and zinc relation : In regulation of food intake and immunity

Attenuation of Gastrointestinal Tract Propulsion in Rats by Zinc Acetate: Investigation into Serotonergic and Dopaminergic Mechanisms

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