Adipokines in critical illness: A review of the evidence and knowledge gaps

Alipoor, Elham; Hosseinzadeh, Fatemeh; Hosseinzadeh‐Attar, Mohammad Javad

doi:10.1016/j.biopha.2018.09.165

Cited by 41 publications

(43 citation statements)

References 141 publications

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“…We determined that the leptin level significantly increased, adiponectin and ghrelin significantly decreased during follow up in PN group, and there were decreased resistin levels as described in catabolic hormones and increased GLP-1 levels as described in anabolic hormones in the EN group. Leptin levels are usually increased due to the rise in endotoxins, certain cytokines, and glucocorticoids in critical illness, although studies of leptin levels are conflicting [4,21]. Leptin is also described as an indicator of fasting or malnutrition [22].…”

Section: Discussionmentioning

confidence: 99%

“…In all studies of resistin, increased levels of blood resistin are powerfully associated with severe inflammation and increased risks of organ failure and mortality [31][32][33]. High ghrelin levels are accepted as a positive predictor 1.0 (0.9-1.2) 0.008 of ICU survival and decreased ghrelin levels can lead to inflammation and length of mechanical ventilation stay [4]. Clinical outcomes due to adipokine levels may differ in artificial nutrition (EN or PN).…”

Section: Discussionmentioning

confidence: 99%

“…Adipose tissue might have an important role in the adaptation to critical illness, which is a multifactorial heterogeneous disease accompanied by inflammation and insulin resistance. It changes the secretory function and leads to major changes in adipokine levels [4]. Therefore, adipokines are suspected of affecting clinical outcomes in critical illness [3,5,6].…”

Section: Introductionmentioning

confidence: 99%

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The association between the route of nutrition and serum levels of adipokines in critical illness: a pilot study

Gündoğan¹,

Doğan²,

Özer³

et al. 2020

Turk J Med Sci

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Background/aim: Adipokines play an important role in the regulation of metabolism. In critical illness, they alter serum levels and are suspected to worsen clinical outcomes. But the effect of the route of nutrition on adipokines is not known. The purpose of this study was to evaluate the association between the route of nutrition and adipokine levels in critically ill patients. Materials and methods: This prospective study was performed in an intensive care unit (ICU). Patients admitted to the ICU for least 72 h and receiving either enteral nutrition (EN) via tube feeding or parenteral nutrition (PN) were enrolled. Serum was obtained at baseline, 24 h, and 72 h for concentrations of leptin, adiponectin, resistin, glucagon-like peptide 1 (GLP-1), insulin-like growth factors 1 (IGF-1), and ghrelin. Results: A total of 26 patients were included in the study. Thirteen patients received EN and 13 patients received PN. In the PN group, leptin level significantly increased (P = 0.037), adiponectin and ghrelin significantly decreased during follow up (P = 0.037, P = 0.008, respectively). There was no significant change between all adipokines in the EN group and resistin, IGF-1 and GLP-1 in the PN group during follow up. Resistin levels were markedly lower in the EN group at both 24 h (P = 0.015) and 72 h (P = 0.006) while GLP-1 levels were higher in the EN group at baseline, 24 h, and 72 h (P = 0.018, P = 0.005, and P = 0.003, respectively). There were no differences in leptin, adiponectin, IGF-1, and ghrelin levels over time. Conclusion: The delivery of EN in critical illness was associated with decreased resistin levels and increased GLP-1 levels. Thus, the route of nutrition may impact the clinical outcome in critical illness due to adipokines.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The association between the route of nutrition and serum levels of adipokines in critical illness: a pilot study

Gündoğan¹,

Doğan²,

Özer³

et al. 2020

Turk J Med Sci

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“…[1][2][3] Furthermore, mature adipocytes produce and release several adipokines throughout the whole body, which are proteins inducing various diseases, such as diabetes mellitus, arteriosclerosis, and hypertension. 4 In particular, angiotensinogen (AGT) secreted from mature adipocytes is one such adipokine; and angiotensin II produced from the AGT via the renin-angiotensin system (RAS) is involved in hypertension. 5 Therefore, we believe that the repression of adipogenesis and a decrease in the number of mature adipocytes should lead to a decreased risk for these diseases.…”

Section: Introductionmentioning

confidence: 99%

Suppression of adipocyte differentiation by low‐intensity pulsed ultrasound via inhibition of insulin signaling and promotion of CCN family protein 2

Nishida

Nagao

Hashitani

et al. 2020

J of Cellular Biochemistry

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Adipocyte differentiation is regulated by several transcription factors such as the CCAAT/enhancer-binding proteins (C/EBPs) and peroxisome proliferatoractivated receptor-γ (PPARγ). Here, we demonstrate that low-intensity pulsed ultrasound (LIPUS) suppressed differentiation into mature adipocytes via multiple signaling pathways. When C3H10T1/2, a mesenchymal stem cell line, was treated with LIPUS (3.0 MHz, 60 mW/cm 2) for 20 minutes once a day for 4 days during adipogenesis, and both the number of lipid droplets and the gene expression of PPARγ and C/EBPα were significantly decreased. Furthermore, LIPUS treatment decreased the phosphorylation of the insulin receptor and also that of Akt and ERK1/2, which are located downstream of this receptor. Next, we showed that LIPUS suppressed the gene expression of angiotensinogen (AGT), which is an adipokine produced by mature adipocytes, as well as that of angiotensinconverting enzyme 1 (ACE1) and angiotensin receptor type 1 (AT 1 R) during adipogenesis of pre-adipogenic 3T3-L1 cells. Next, the translocation of Yesassociated protein (YAP) into the nucleus of 3T3-L1 cells was promoted by LIPUS, leading to upregulation of CCN family protein 2 (CCN2), a cellular communication network factor. Moreover, forced expression of CCN2 in 3T3-L1 cells decreased PPARγ gene expression, but it did not increase alkaline phosphatase and osterix gene expression. Finally, gene silencing of CCN2 in C3H10T1/2 cells diminished the effect of LIPUS on the gene expression of PPARγ and C/EBPα. These findings suggest that LIPUS suppressed adipogenesis through inhibition of insulin signaling and decreased PPARγ expression via increased CCN2 production, resulting in a possible decrease of mature adipocytes.

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“…The endocrine function of adipose tissue, changes in adipokines and the gaps of knowledge in critical illness have been recently reviewed elsewhere. 10 White adipose tissue (WAT) browning is a recent topic of interest in obesity and associated disorders. Accumulating evidence suggests that changes in the fundamental morphologic, physiologic and metabolic activity of adipose tissue 11 along with browning of white adipocytes 12 can influence outcomes in critical illness.…”

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confidence: 99%

White adipose tissue browning in critical illness: A review of the evidence, mechanisms and future perspectives

et al. 2020

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Observational studies suggest better clinical outcomes following critical illness in patients with overweight and obesity (obesity paradox). An understanding of the morphologic, physiologic and metabolic changes in adipose tissue in critical illness may provide an explanation. Recent studies have demonstrated the transformation of white to brown-like adipocytes due to the "browning process," which has been of interest as a potential novel therapy in obesity during the last decade. The characteristics of the browning of white adipose tissue (WAT) include the appearance of smaller, multilocular adipocytes, increased UCP1 mRNA expression, mitochondrial density and respiratory capacity. These changes have been identified in some critical illnesses, which specifically refers to burns, sepsis and cancer cachexia in this study. The pathophysiological nature of WAT browning, underlying mechanisms, main regulators and potential benefits and harms of this process are interesting new areas that warrants further investigations. In this review, we discuss emerging scientific discipline of adipose tissue physiology in metabolic stress, available data, gaps of knowledge and future perspectives. Future investigations in this field may provide insights into the underlying mechanisms and clinical aspects of browning that may further our understanding of the proposed obesity paradox following critical illness, which may in turn open up opportunities for novel therapies to save lives and improve recovery.

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Adipokines in critical illness: A review of the evidence and knowledge gaps

Cited by 41 publications

References 141 publications

The association between the route of nutrition and serum levels of adipokines in critical illness: a pilot study

The association between the route of nutrition and serum levels of adipokines in critical illness: a pilot study

Suppression of adipocyte differentiation by low‐intensity pulsed ultrasound via inhibition of insulin signaling and promotion of CCN family protein 2

White adipose tissue browning in critical illness: A review of the evidence, mechanisms and future perspectives

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