Adiponectin signaling in the liver

Combs, Terry P.; Marliss, Errol B.

doi:10.1007/s11154-013-9280-6

Cited by 133 publications

(100 citation statements)

References 97 publications

(126 reference statements)

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“…Liver triglyceride content did not correlate with serum triglyceride levels in APNko-DHT mice, while APNtg mice had lower circulating triglycerides. There may be multiple protective effects of adiponectin on hepatic steatosis and hypertriglyceridemia, including direct action on the liver, improved capacity for safe deposition of excess nutrients in the s.c. fat compartment, and an increased metabolic activity in BAT (16,17,(42)(43)(44).…”

Section: Discussionmentioning

confidence: 99%

Adiponectin protects against development of metabolic disturbances in a PCOS mouse model

Benrick

Chanclón

Micallef

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Adiponectin, together with adipocyte size, is the strongest factor associated with insulin resistance in women with polycystic ovary syndrome (PCOS). This study investigates the causal relationship between adiponectin levels and metabolic and reproductive functions in PCOS. Prepubertal mice overexpressing adiponectin from adipose tissue (APNtg), adiponectin knockouts (APNko), and their wild-type (WT) littermate mice were continuously exposed to placebo or dihydrotestosterone (DHT) to induce PCOS-like traits. As expected, DHT exposure led to reproductive dysfunction, as judged by continuous anestrus, smaller ovaries with a decreased number of corpus luteum, and an increased number of cystic/atretic follicles. A two-way between-groups analysis showed that there was a significant main effect for DHT exposure, but not for genotype, indicating adiponectin does not influence follicle development. Adiponectin had, however, some protective effects on ovarian function. Similar to in many women with PCOS, DHT exposure led to reduced adiponectin levels, larger adipocyte size, and reduced insulin sensitivity in WTs. APNtg mice remained metabolically healthy despite DHT exposure, while APNko-DHT mice were even more insulin resistant than their DHT-exposed littermate WTs. DHT exposure also reduced the mRNA expression of genes involved in metabolic pathways in gonadal adipose tissue of WT and APNko, but this effect of DHT was not observed in APNtg mice. Moreover, APNtg-DHT mice displayed increased pancreatic mRNA levels of insulin receptors, Pdx1 and Igf1R, suggesting adiponectin stimulates beta cell viability/hyperplasia in the context of PCOS. In conclusion, adiponectin improves metabolic health but has only minor effects on reproductive functions in this PCOS-like mouse model. polycystic ovary syndrome | insulin resistance | adipose tissue P olycystic ovary syndrome (PCOS) is the most common endocrine and metabolic disorder occurring in females (1). PCOS is one of the leading causes of poor fertility and is associated with abdominal obesity, metabolic syndrome, and an increased risk of developing type 2 diabetes (1, 2). Indeed, it has been demonstrated that 30-40% of women with PCOS have impaired glucose tolerance, and as many as 10% develop diabetes by the age of 40 y (3, 4). Despite the negative effect of PCOS on women's health, very little is known about its etiology, including the causal relationship between the reproductive and metabolic features of PCOS. Adipose tissue dysfunction is implicated as a key feature, and both lean and obese women with PCOS have aberrant adipose tissue morphology (5-7). Specifically, we have found that large adipocyte size, low circulating adiponectin levels, and increased waist circumference, but surprisingly, not androgen excess, are factors that are most strongly associated with insulin resistance in women with PCOS (8). Others have shown that hyperandrogenism is associated with intra-abdominal fat deposition (9). Adiponectin is an adipocyte-derived hormone exerting potent positive effec...

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Section: Discussionmentioning

confidence: 99%

Adiponectin protects against development of metabolic disturbances in a PCOS mouse model

Benrick

Chanclón

Micallef

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…Metabolic regulation and maintenance of whole-body energy homeostasis are considered the main physiological roles of adiponectin, and it is generally accepted that the primary target organs of adiponectin are the liver and skeletal muscle [12]. Other major physiological activities of adiponectin include anti-inflammatory and anti-apoptotic effects [13,14].…”

Section: Introductionmentioning

confidence: 99%

The Activity of Adiponectin in Bone

2016

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The adipokine adiponectin affects multiple target tissues and plays important roles in glucose metabolism and whole-body energy homeostasis. Circulating adiponectin levels in obese people are lower than in non-obese, and increased serum adiponectin is associated with weight loss. Numerous clinical studies have established that fat mass is positively related to bone mass, a relationship that is maintained by communication between the two tissues through hormones and cytokines. Since adiponectin levels inversely correspond to fat mass, its bone effects and its potential contribution to the relationship between fat and bone have been investigated. In clinical observational studies, adiponectin was found to be negatively associated with bone mineral density, suggesting it might be a negative regulator of bone metabolism. In order to identify the mechanisms that underlie the activity of adiponectin in bone, a large number of laboratory studies in vitro and in animal models of mice over-expressing or deficient of adiponectin have been carried out. Results of these studies are not entirely congruent, partly due to variation among experimental systems and partly due to the complex nature of adiponectin signaling, which involves a combination of multiple direct and indirect mechanisms.

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“…Pregnancy needs to meets the energy requirements by the development of fetus this intern need aspecial dynamic rearrangements of adipose tissue activity which is usually associated with an initial period of adipogenesis followed by increase lipolytic activity (19) , the present study showed that quantitative expression of adiponectin receptor 2 in adipocytes was less than those recorded a non pregnant (control group) and this result respond to be in approval with many other studies than by different authers that discripe changes of adiponectin during pregnancy and showed the progressive decline of plasma adiponectin that in pregnancy advanced. (20,21,22) Opposite it to the non-pregnant state adiponectin level so out pregnancy it is not correlated to maternal body mass index, however there is the distraction of the correlation between the adiponectin and maternal weight can results were form several factors the most appaling cause for this description this dramtic for hormonal changes during pregnancy total body weight showed (33.15 ± 0.57g) in pregnant group and (29.08 ± 0.55g) non-pregnant group in a study done by (23) , basic metabolic was study investigated in for hand pregnant women in relation in the pregnancy trimesters. Maternal characteristics of plasma adiponectin consentration showed a significant decrease in the level of serum adiponectin with the advanced pregnancy gestational age and the increase body mass index the over all analysis of level of adiponectin in pregnant and non-pregnant group showed a slightly statistical significant decrease in level of plasma adiponectin concentration with advancing gestational age but significant difference between in the three trimesters were not found.…”

Section: Cmentioning

confidence: 99%

“…However, considering the breakdown of the adiponectin signaling pathway in T1D, the development of medications that stimulate the production of SOGA directly could restore the metabolic balance, diminish the insulin requirement and improve clinical outcomes. (21) The parallel changes in total plasma adiponectin and adipose tissue adiponectin gene expression argue in favour of plasma adiponectin levels reflecting pregnancy-associated adiponectin production. Whether the regulation is at the transcriptional or translational level or at the level of secretion into the systemic circulation is not known.…”

Section: Cmentioning

confidence: 99%