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

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].

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