Novel insights into the relationship between nonalcoholic fatty liver disease and osteoporosis

Filip, Rafał; Radzki, Radosław P.; Bieńko, Marek

doi:10.2147/cia.s170533

Cited by 45 publications

(31 citation statements)

References 141 publications

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“…Regarding a possible influence of the FF metabolic state on enhancing bone mass, evidence indicates the opposite. Specifically, fatty liver disease does not increase bone mass and in fact, promotes osteoporosis [31]. Moreover the bone mass of high fat-fed, insulin-resistant C57/BL6 mice is also decreased due to arrested bone formation [32].…”

Section: Discussionmentioning

confidence: 99%

Congenital lipodystrophy induces severe osteosclerosis

et al. 2019

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Berardinelli-Seip congenital generalized lipodystrophy is associated with increased bone mass suggesting that fat tissue regulates the skeleton. Because there is little mechanistic information regarding this issue, we generated "fat-free" (FF) mice completely lacking visible visceral, subcutaneous and brown fat. Due to robust osteoblastic activity, trabecular and cortical bone volume is markedly enhanced in these animals. FF mice, like Berardinelli-Seip patients, are diabetic but normalization of glucose tolerance and significant reduction in circulating insulin fails to alter their skeletal phenotype. Importantly, the skeletal phenotype of FF mice is completely rescued by transplantation of adipocyte precursors or white or brown fat depots, indicating that adipocyte derived products regulate bone mass. Confirming such is the case, transplantation of fat derived from adiponectin and leptin double knockout mice, unlike that obtained from their WT counterparts, fails to normalize FF bone. These observations suggest a paucity of leptin and adiponectin may contribute to the increased bone mass of Berardinelli-Seip patients.

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Section: Discussionmentioning

confidence: 99%

Congenital lipodystrophy induces severe osteosclerosis

et al. 2019

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“…93 Chronic inflammation, vitamin D3, growth hormone, insulin-like growth factor 1, osteopontin, fetuin-A, irisin, osteocalcin, and osteoprotegerin from osteoblasts have been proposed as mediators of mutual interactions among the skeleton, fatty tissue, and liver leading to osteoporosis. 94 A study from Italy has shown independent associations between (a) low BMD and PNPLA3 CG + GG genotype; (b) low BMD and NASH; and (c) PNPLA3 CG + GG genotype and NASH, providing support for a causal relationship between NASH and low BMD. 95 An earlier meta-analysis concluded that there is controversy regarding the effect of NAFLD on BMD.…”

Section: ) Osteoporosis/osteopeniamentioning

confidence: 99%

Magnitude of Nonalcoholic Fatty Liver Disease: Western Perspective

Samji

Verma

Satapathy

2019

Journal of Clinical and Experimental Hepatology

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The incidence of nonalcoholic fatty liver disease (NAFLD) is continuing to rise worldwide, and it is estimated that this disquieting trend will continue for another 10-15 years before prevalence begins to decrease. NAFLD is the hepatic manifestation of metabolic syndrome. As obesity, diabetes, and other lifestyle-related diseases continue to rise, the spectrum of NAFLD, e.g., nonalcoholic steatohepatitis, liver fibrosis, liver cirrhosis, liverrelated morbidity, and mortality, will increase in parallel. Its widespread prevalence and associated economic burden have drawn significant attention, and a multitude of pharmaceutical companies are participating in active research trying to find a "cure". Unfortunately, as of now, no targeted treatment exists to treat this condition, and therefore, emphasis has been on its prevention. The current review focuses on the epidemiology, clinical characteristics, risk factors, and clinical outcomes of NAFLD in Western countries. It is important to understand the magnitude of NAFLD and its risk factors in Western countries where the prevalence of NAFLD has now reached epidemic proportions to identify the best strategy to prevent and possibly control this epidemic.

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“…Proven links between NAFLD and decreased bone mass include vitamin D insufficiency 96 , the growth hormone/IGF-I axis 97 , TNF-α 98 , the receptor activator of NF-κB (RANK)/osteoprotegerin pathway 99 , fetuin-A 100 , osteopontin 101 , and adiponectin 102 . In addition, chronic inflammation and irisin from osteoblasts have been proposed as mediators of mutual interactions among the skeleton, fatty tissue, and liver 103 . Patients with ALD often have accompanying decreased vitamin D levels, which is primarily attributed to reduced hepatic 25-hydroxylase activity, malabsorption, irregular feeding habits and lack of sun exposure 104 .…”

Section: Communications Between the Liver And Other Major Organsmentioning

confidence: 99%

Organ-organ communication: The liver's perspective

Wang¹,

So²,

Xiao³

et al. 2021

Theranostics

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Communication between organs participates in most physiological and pathological events. Owing to the importance of precise coordination among the liver and virtually all organs in the body for the maintenance of homeostasis, many hepatic disorders originate from impaired organ-organ communication, resulting in concomitant pathological phenotypes of distant organs. Hepatokines are proteins that are predominantly secreted from the liver, and many hepatokines and several signaling proteins have been linked to diseases of other organs, such as the heart, muscle, bone, and eyes. Although liver-centered interorgan communication has been proposed in both basic and clinical studies, to date, the regulatory mechanisms of hepatokine production, secretion, and reciprocation with signaling factors from other organs are obscure. Whether other hormones and cytokines are involved in such communication also warrants investigation. Herein, we summarize the current knowledge of organ-organ communication phenotypes in a variety of diseases and the possible involvement of hepatokines and/or other important signaling factors. This provides novel insight into the underlying roles and mechanisms of liver-originated signal transduction and, more importantly, the understanding of disease in an integrative view.

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Novel insights into the relationship between nonalcoholic fatty liver disease and osteoporosis

Cited by 45 publications

References 141 publications

Congenital lipodystrophy induces severe osteosclerosis

Congenital lipodystrophy induces severe osteosclerosis

Magnitude of Nonalcoholic Fatty Liver Disease: Western Perspective

Organ-organ communication: The liver's perspective

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