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Table 2 Evidence for the role of novel adipokines in mediating insulin sensitivity

From: The role of adipokines in skeletal muscle inflammation and insulin sensitivity

Adipokine Association with obesity and/or T2D in humans Adipokine effect on insulin signalling in animal models Adipokine effect on insulin signalling in human skeletal muscle
   In Vivo In Vitro  
FGF-21 Increased [86]. Increased insulin sensitivity and glucose uptake in mice, via FGF-21 mediated increases in adiponectin production and secretion from adipocytes [76]. 6 h incubation of mouse EDL muscle with FGF-21 resulted in a 54% increase in insulin stimulated glucose uptake [86]. Directly increased glucose uptake in primary human myotubes [86].
Prevents palmitate-induced insulin resistance in primary human myotubes by inhibiting stress kinases and NF-κB [87].
   Continuous cerebral administration for 2 weeks increased whole body insulin sensitivity in rats with dietary induced obesity [77].   
   Daily administration for 6 weeks improved glucose handling in diabetic rhesus monkeys [78].   
Chemerin Increased [94, 138]. Overexpression increased insulin resistance in LDL receptor deficient mice by reducing AKT phosphorylation in response to insulin in skeletal muscle, but not liver or pancreas [96]. 24 h pre-treatment reduces insulin stimulated glucose uptake in C2C12 myotubes in a dose dependent manor [99]. 24 h chemerin Increased insulin resistance and reduced insulin stimulated glucose uptake in primary human myotubes, mediated by increased ERK signalling [95].
  knockout mice display increased skeletal muscle insulin resistance while transgenic mice exhibit increased skeletal muscle insulin resistance [98].
   Acute chemerin treatment exacerbated glucose intolerance and lowered serum insulin levels in obese and diabetic mice. No effect observed in normoglycemic mice [97].
CTRP3 Decreased [115, 116, 139]. Administration of recombinant CTRP3 directly lowers glucose levels in normal and insulin-resistant ob/ob mice [140]. Administration of recombinant CTRP3 to L6 myotubes had no effect on glucose uptake [140]. Unknown
Overexpression of CTRP3 improved insulin sensitivity in HFD fed mice [141]. Increased glucose uptake and GLUT 4 mRNA expression in insulin resistant adipocytes [142].
RBP4 Increased [143, 144]. Overexpression or direct administration of RBP4 increased insulin resistance in mice. RBP4 knockout improves insulin sensitivity in mice [144]. unknown Unknown
Reducing circulating RBP4 in obese mice models improved glucose tolerance and increased insulin stimulated glucose uptake in skeletal muscle up to 60% [145].
Vaspin Increased [65, 67, 68]. Vaspin treatment increased insulin sensitivity and glucose tolerance in obese and diabetic mice [59, 60]. Unknown Unknown
transgenic mice overexpressing vaspin displayed improved glucose tolerance and were protected from obesity when challenged with a high fat diet [62].   
Pref-1 Increased [101]. Overexpression in mice drives insulin resistance via decreased adipose tissue and skeletal muscle glucose uptake and impaired skeletal muscle insulin signalling [105]. Unknown 4 Day exposure to primary human myotubes from lean, obese and T2D subjects had no effect on glucose uptake [106].
Follistatin-like 1 Increased [108]. Unknown Blunts insulin signalling-adipocytes [108]. unknown
Omentin-1 Decreased [146, 147]. Unknown omentin-1 induced AKT phosphorylation and enhanced insulin-stimulated glucose uptake in human adipocytes [123]. Unknown
Unknown
Lipocallin-14 Unknown Over expression in diet induced obese mice reduced glucose and insulin levels while improving glucose tolerance [124]. Unknown