Age- and Tissue-Dependent Modulation of IGF-1/PI3K/Akt Protein Expression by Dietary Restriction in Mice

Hadem, Ibanylla Kynjai Hynniewta; Sharma, Ramesh

doi:10.1055/s-0035-1559770

Cited by 14 publications

(12 citation statements)

References 30 publications

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“…Previous studies have already revealed various critical mediators and signaling pathways involved in CR . One major pathway is the GH/IGF‐1/insulin axis (growth hormone/insulin growth factor 1/insulin) . In CR‐fed mice or patients under CR or anorexia, reduced IGF‐1 serum levels have been reported .…”

Section: Discussionmentioning

confidence: 99%

“…(44) One major pathway is the GH/IGF-1/insulin axis (growth hormone/ insulin growth factor 1/insulin). (23,(44)(45)(46)(47)(48)(49) In CR-fed mice or patients under CR or anorexia, reduced IGF-1 serum levels have been reported. (23,28,(46)(47)(48)(49) Interestingly, early-life loss of IGF-1 in female mice resulted in a 67% increase in vertebral bone volume fraction, as well as enhanced connectivity density and trabecular number at 27 months of age in a recent murine study of Ashpole.…”

Section: Discussionmentioning

confidence: 99%

“…(23,(44)(45)(46)(47)(48)(49) In CR-fed mice or patients under CR or anorexia, reduced IGF-1 serum levels have been reported. (23,28,(46)(47)(48)(49) Interestingly, early-life loss of IGF-1 in female mice resulted in a 67% increase in vertebral bone volume fraction, as well as enhanced connectivity density and trabecular number at 27 months of age in a recent murine study of Ashpole. (50) Hence, decreased IGF-1 signaling might also be present in our study, especially because Hamrick and colleagues detected reduced serum leptin and IGF-1 levels in a comparative CR approach (28) together with comparable different action of CR on cortical and trabecular bone as shown in the present study.…”

Section: Discussionmentioning

confidence: 99%

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Dietary Restriction-Induced Alterations in Bone Phenotype: Effects of Lifelong Versus Short-Term Caloric Restriction on Femoral and Vertebral Bone in C57BL/6 Mice

Behrendt

Kuhla

Osterberg

et al. 2015

Journal of Bone and Mineral Research

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Caloric restriction (CR) is a well-described dietary intervention that delays the onset of aging-associated biochemical and physiological changes, thereby extending the life span of rodents. The influence of CR on metabolism, strength, and morphology of bone has been controversially discussed in literature. Thus, the present study evaluated whether lifelong CR versus short-term late-onset dietary intervention differentially affects the development of senile osteoporosis in C57BL/6 mice. Two different dietary regimens with 40% food restriction were performed: lifelong CR starting in 4-week-old mice was maintained for 4, 20, or 74 weeks. In contrast, short-term late-onset CR lasting a period of 12 weeks was commenced at 48 or 68 weeks of age. Control mice were fed ad libitum (AL). Bone specimens were assessed using microcomputed tomography (mCT, femur and lumbar vertebral body) and biomechanical testing (femur). Adverse effects of CR, including reduced cortical bone mineral density (Ct.BMD) and thickness (Ct.Th), were detected to some extent in senile mice (68þ12w) but in particular in cortical bone of young growing mice (4þ4w), associated with reduced femoral failure force (F). However, we observed a profound capacity of bone to compensate these deleterious changes of minor nutrition with increasing age presumably via reorganization of trabecular bone. Especially in lumbar vertebrae, lifelong CR lasting 20 or 74 weeks had beneficial effects on trabecular bone mineral density (Tb.BMD), bone volume fraction (BV/TV), and trabecular number (Tb.N). In parallel, lifelong CR groups showed reduced structure model index values compared to age-matched controls indicating a transformation of vertebral trabecular bone microarchitecture toward a platelike geometry. This effect was not visible in senile mice after short-term 12-week CR. In summary, CR has differential effects on cortical and trabecular bone dependent on bone localization and starting age. Our study underlines that bone compartments possess a lifelong capability to cope with changing nutritional influences.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Dietary Restriction-Induced Alterations in Bone Phenotype: Effects of Lifelong Versus Short-Term Caloric Restriction on Femoral and Vertebral Bone in C57BL/6 Mice

Behrendt

Kuhla

Osterberg

et al. 2015

Journal of Bone and Mineral Research

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“…Indeed, evidence from studies in kidneys of aged male C57Bl/6 mice (> 18 months) demonstrated that aging reduces the normal proliferative responses that follow an acute insult to renal tubular cells (Schmitt 2006; Berkenkamp et al 2014). Analyses of kidneys from older human subjects (> 71 years) showed that renal levels of cytokines such as insulin-like growth factor-1 (IGF-1) and epidermal growth factor (EGF) (Chou et al 1997; Shurin et al 2007; Hadem and Sharma 2016), which play roles in cell proliferation, decrease as humans age. The reduction in these cytokines may be an important factor in the inability of aged kidneys to initiate efficient cellular repair mechanisms.…”

Section: Aging and The Normal Kidneysmentioning

confidence: 99%

The aging kidney and the nephrotoxic effects of mercury

Bridges

Zalups

2017

Journal of Toxicology and Environmental Health, Part B

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Owing to advances in modern medicine, life expectancies are lengthening and leading to an increase in the population of older individuals. The aging process leads to significant alterations in many organ systems, with the kidney being particularly susceptible to age-related changes. Within the kidney, aging leads to ultrastructural changes such as glomerular and tubular hypertrophy, glomerulosclerosis, and tubulointerstitial fibrosis, which may compromise renal plasma flow (RPF) and glomerular filtration rate (GFR). These alterations may reduce the functional reserve of the kidneys making them more susceptible to pathological events when challenged or stressed, such as following exposure to nephrotoxicants. An important and prevalent environmental toxicant that induces nephrotoxic effects is mercury (Hg). Since, exposure of normal kidneys to mercuric ions might induce glomerular and tubular injury, aged kidneys, which may not be functioning at full capacity, may be more sensitive to the effects of Hg than normal kidneys. Age-related renal changes and the effects of Hg in the kidney have been characterized separately. However, little is known regarding the influence of nephrotoxicants, such as Hg, on aged kidneys. The purpose of this review was to summarize known findings related to exposure of aged and diseased kidneys to the environmentally relevant nephrotoxicant, Hg.

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“…First, we did not test the effect of other hormones that may also influence bone metabolism, such as IGF-1 and fibroblast grow factor 21 (FGF21). [30][31][32][33] Above all, IGF-1 has been proposed as a key molecule for the stress resistance, life-prolonging, and anticancer actions of CR, 2,34 in addition to molecules, such as hydrogen sulfide. 35 Moreover, many studies have shown that IGF-1 is important for normal bone development in growing mice.…”

Section: Discussionmentioning

confidence: 99%

Short‐term caloric restriction induced bone loss in both axial and appendicular bones by increasing adiponectin

Zhu

Liu

Jia

et al. 2020

Annals of the New York Academy of Sciences

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Caloric restriction (CR) is well described and has received extensive attention for its multiple benefits, including longevity and stress resistance. However, some studies have shown that CR negatively influences bone, although a mechanism hasn't been provided. Adiponectin, an adipocyte‐derived hormone, can affect bone metabolism by various pathways. To explore the role of adiponectin in short‐term CR on bone, we tested the effect of short‐term CR on limb bones (tibia and femur) and lumbar vertebral bodies of young C57BL/6 wild‐type (WT) and adiponectin‐deficient (Apn–/–) mice. Two dietary regimes, ad libitum (AL) and CR (70% of the AL diet), were used. Dietary restriction led to increased serum adiponectin in WT mice, while bone mineral density, bone microarchitecture, and biomechanical outcomes of limb bone and vertebrae were decreased. In contrast, bone length, microarchitecture, and biomechanical outcomes were not impaired after CR in Apn–/– mice. Furthermore, CR increased adiponectin expression both in white adipose tissue and bone marrow adipose tissue in young WT mice. Histology analysis showed that expansion of bone marrow adipose tissue after CR in Apn–/– mice was impaired compared with WT mice. These results suggest that increased adiponectin induced by short‐term CR may negatively influence bones.

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Age- and Tissue-Dependent Modulation of IGF-1/PI3K/Akt Protein Expression by Dietary Restriction in Mice

Cited by 14 publications

References 30 publications

Dietary Restriction-Induced Alterations in Bone Phenotype: Effects of Lifelong Versus Short-Term Caloric Restriction on Femoral and Vertebral Bone in C57BL/6 Mice

Dietary Restriction-Induced Alterations in Bone Phenotype: Effects of Lifelong Versus Short-Term Caloric Restriction on Femoral and Vertebral Bone in C57BL/6 Mice

The aging kidney and the nephrotoxic effects of mercury

Short‐term caloric restriction induced bone loss in both axial and appendicular bones by increasing adiponectin

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