Plasma MiR-106a-5p (miR-17) MiR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, miR-363 ↑

Down-regulated in polycystic ovary syndrome (PCOS)36

Elevated in aged muscles (mice) and dexamethasone-treated myotubes; agomir results in down-regulation of both myogenic regulatory factors (MyoD, MyoG, and MyHC) and phosphorylation of AKT and decreased myotube size37

Plasma exosomes36

C2C12 cells37

Mice37

PIK3R137 MiR-1224-5p (miR-1224) N/A ↑ Up-regulated in the liver of obese and high-fat diet-fed mice, contributes to hepatic lipid accumulation by targeting AMPKα138 Mice38 AMPKα138 MiR-1246 (miR-1246) N/A ↑

Down-regulated in patients with chronic obstructive pulmonary disease (COPD) and emphysema (n = 20)39 and amyotrophic lateral sclerosis (ALS) patients (n = 14)40

Up-regulated in diabetic nephropathy patients (n = 23); positively correlated with BMI41

Serum39, 41

Plasma40

MiR-145-5p (miR-145) MiR-145, miR-143 ↑

Limited studies on obesity/sarcopenia

Up-regulated in normal-weight women (n = 11) following a high-energy/fat breakfast42

Plasma42 MiR-18b-5p (miR-17) MiR-106a, miR-18b, miR-20b, miR-19b-2, miR-92a-2, miR-363 ↑

Limited studies on obesity/sarcopenia

Up-regulated in PCOS43 and relapsing multiple sclerosis (MS), may be involved in inflammatory pathways44

SORBS2 identified as a target in diabetic nephropathy model cells45

Targets and inhibits IGF-1, suppressing the activation of p-AKT, p-MEK, and p-ERK1/2 in vitro46

Serum43, 44

HGMCs/HRGECs45

HRECs46

SORBS245

IGF-146

MiR-193b-5p (miR-193) MiR-193b, miR-365a ↑

Limited studies on obesity/sarcopenia

Weak negative correlations with BMI, plasma glucose levels, and insulin response to OGTT in younger adults47

Targets and decreases expression of FoxO3 in cells, regulating cell cycle and cell proliferation48

Subcutaneous adipose tissue47

BRL-3A48

FoxO348 MiR-196a-5p (miR-196) N/A ↑ High level of expression in myoblasts, suppresses mitochondrial biogenesis and its master regulator, PGC1β, and ND4. Suppresses osteoclast formation induced by RANKL in Raw264.7 cells49

C2C12 cells49

Raw264.7 cells49

MiR-197-3p (miR-197) N/A ↑

Increased after high-intensity resistance exercise in young adults50

Up-regulation inhibits GIP and GLP-1 production through suppression of PCSK1/350

Serum50

STC-1 cells51

MiR-199a-5p (miR-199) MiR-214 ↓

Overexpression of AKT down-regulates miR-199a-5p with a subsequent increase in targets Sirt1 and HiF-1α in cardiomyocytes52

Down-regulated in mild and terminal-stage ALS53 and patients with Parkinson's disease54

Up-regulated in middle-aged adults with T2DM; in vitro studies showed that miR-199a regulates cellular glucose uptake by targeting and suppressing GLUT455

Up-regulated in rat pancreatic β-cells exposed to high glucose, promotes apoptosis and ROS formation, suppresses SIRT156

Inhibition results in decreased myogenic differentiation and increased MyoD1 and Pax7 in human myoblasts. High levels inhibit WNT signalling in HEK293T cells. Overexpression in zebrafish results in disorganization and detachment of myofibres57

Cardiomyocytes52

Serum53

Plasma55

Induced pluripotent stem cells54

Rat pancreatic β-cells56

Myoblasts, HEK293T cells, zebrafish57

Sirt152, 56, 58

HiF-1α52

GLUT455

MiR-296-3p (miR-296) MiR-296, miR-298 ↑ Up-regulated in PCOS; reduction in miR-296-3p promotes cell proliferation59

Human granulosa cells59

Human granulosa-like tumour cells59

PTEN59 MiR-29b-2-5p (miR-29) MiR-29b-2, miR-29c ↑

Limited studies in the context of muscle/obesity

Targets STAT3 in a fibroblast cell line60

L929 cells60 STAT360 MiR-301b-3p (miR-130) MiR-301b, miR-130 ↓ Decreased during myogenic differentiation; may be involved in muscle differentiation by regulating Rb1cc161 Chicken myoblasts61 Rb1cc161 MiR-378c N/A ↑ Studies not identified in the context of muscle/obesity MiR-4732-5p (miR-4732) MiR-4732, miR-144, miR-451a, miR-451b ↑ Studies not identified in the context of muscle/obesity MiR-483-3p (miR-483) N/A ↑

Up-regulated in hyperglycaemic mice and cardiomyocytes. Overexpression down-regulates IGF-1, thus promoting apoptosis in hyperglycaemic cardiomyocytes62

Overexpression inhibits bovine myoblast cell proliferation through the IGF1/PI3K/AKT pathway; knockdown of miR-483 enhances the expression of myogenic maker genes MyoD1, MyoG, and MyHC63

Elevated in Duchenne's muscular dystrophy64

Mice, H9c2 cell line62

Bovine myoblasts63

Serum64

IGF-162, 63 MiR-487a-3p (miR-154) MiR-1185-1, miR-1185-2, miR-381, miR-487a, miR-487b, miR-539, miR-889, miR-544a, miR-655, miR-382, miR-154, miR-496, miR-377, miR-134, miR-668, miR-485, miR-323b ↓ Studies not identified in the context of muscle/obesity MiR-499a (miR-499) MyomiR

MiR-499a, miR-499b

Encoded in slow myosin heavy chain genes (Myh7b)—restricted to T1 fibres (expressed in T1 fibres only)

↓

Elevated in patients and carriers (mothers) with Duchenne's muscular dystrophy65 and COPD (n = 103) and significantly correlated with NF-κB p5066

Affected by aerobic exercise—no changes after acute bout in young men67; decreased following acute bout with weight vest with/without nutritional supplementation68; increased in male marathon runners (n = 21) after competitive marathon competition69

Increased after essential amino acid (EAA) ingestion in young adults (n = 7)70

Associated with a slow muscle fibre phenotype in human muscle71

Double knockout miR-499/miR-208b mice lost slow Type I myofibres with a concomitant increase in fast Type IIx/d and IIb myosin isoforms; forced expression of miR-499 converted fast myofibres to slow. Sox6 helps mediate the actions of miR-499 on slow myofibre gene programming72

Targets Thrap1 to promote slow muscle fibre type73

Targets TGF-βR1, a known regulator of skeletal myoblast development. Knockdown of TGF-βR1 inhibits myogenic differentiation in C2C12 cells74

Targets PRDM16, which subsequently promotes myogenic, rather than brown adipogenic, differentiation in mouse skeletal muscle stem cells (SMSCs)75

Promotes mitochondrial function. Targets Fnip1, a negative regulator of mitochondrial function in myocytes, which leads to activation of PGC-1α. Fnip1 inhibition stimulates oxygen consumption rates, a sign of mitochondrial function, in myocytes. Mice with muscular dystrophy bred with miR-499 mice exhibit improved mitochondrial capacity, restored slow-oxidative muscle fibre programming and greater muscle functionality assessed with treadmill distance76

Knockdown of p21, a target of miR-499, decreases mitochondrial fission and cell death in cardiomyocytes exposed to doxorubicin, anti-tumour drug77

PTENP1, a target gene of miR-499, expression is enhanced in diabetic and obese mouse models resulting in impaired AKT/GSK activation and glycogen synthesis contributing to insulin resistance78

Down-regulation was observed in diabetic mouse models. Down-regulation in vitro was shown to impair the insulin signalling, AKT/GSK pathway and glycogen synthesis. PTEN was identified as a target79

Plasma65, 66, 69

Serum67

Vastus lateralis68, 70, 71

Mice71, 72, 76-79

C2C12 cells72-74

SMSCs75

H9c2 cells77

Murine liver cells NCTC146978, 79

Sox672

Thrap172, 73

p2177

TGF-βR174

PRDM1675

Fnip176

PTEN79

PTENP178

MiR-550a-3p (miR-550) MiR-550a-1, miR-550b-1 ↑

Limited studies in muscle/obesity

Down-regulated in patients with sporadic ALS80

Associated with parameters of bone formation and microstructure parameters (mineral apposition ratio, bone surface, trabecular bone volume)81

Down-regulated in postmenopausal women with fractures older than 6 months; excellent discrimination of patients with low traumatic fractures82

Peripheral blood80

Serum81, 82

MiR-576-5p (miR-576) N/A ↑ Studies not identified in the context of muscle/obesity MiR-589-5p (miR-589) N/A ↑

Limited studies in muscle/obesity

Decreased upon TGF-β stimulation in control fibroblasts, with no effect seen in COPD fibroblasts83

Fibroblasts83 MiR-766-3p (miR-766) N/A ↑

Decreased in older (60–73 years; n = 51) compared with younger (19–42 years; n = 55) or long-lived (90–102 years; n = 51) adults.84 Overexpressed in older adult human dermal fibroblasts (HDFs)85

Decreased after 12 weeks of endurance training in young men (n = 32)86

Increased in sedentary T2DM adults (40–70 years; n = 24) who undertook either 4 month resistance or aerobic training87

PBMCs84

HDFs85

HeLa cells85

Plasma86, 87

SIRT685 MiR-92a-3p (miR-92a)

MiR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, miR-92a-1

↑

Anti-miR, MRG-110, was tested in adult men and found to counteract the repression of known miR-92a-3p targets, ITGA5 and CD93. Elevated levels of DDIT4, an inhibitor of mTOR, were found in cells treated with MRG-11088

In a systematic review, down-regulated following bariatric surgery89

Decreased following 20 week aerobic exercise training (n = 20),90 12 week endurance training in young men (n = 32),86 and a 6 week cycling training in young men (n = 24)91

No change following 5 month aerobic training in obese older adults (n = 33); however changes in miR-92a positively correlated with changes in gait speed following intervention92

MiR-92a targets SMAD7, inhibition of miR-92a led to increased mitochondrial content and oxygen consumption of brown adipocytes; inhibition of miR-92a led to promotion of SMAD7 and subsequent suppression of p-SMAD3/SMAD3. Inhibition of miR-92a promoted differentiation of brown adipocytes.93 Negatively correlated with BAT activity in young adults (n = 41); down-regulated in the serum exosomes of mice with active BAT94

Gradually up-regulated with age (22, 40, 59, and 70 years) in men and women95

Whole blood88

CD4+ T cells88

Plasma86, 89, 92

Serum90, 94, 95

C2C12 cells93

Vastus lateralis91

Mice94

ITGA588

CD9388

SMAD793

Serum MiR-23a-3p (miR-23) Mir-23a, miR-27a, miR-24-2 ↑

Significantly down-regulated in SAT and VAT of obese participants and significantly correlated with measures of adiposity (BMI, waist circumference, insulin measures). Involved in the regulation of PTEN, although the molecular mechanism is unclear96

In young men (n = 7), increased following resistance or endurance exercise and protein ingestion97

Increased following EAA ingestion alone70

Decreased after an acute bout of endurance exercise in young adults (n = 9)98

Up-regulated in ALS. Targets PGC-1α with subsequent effects on mitochondrial biogenesis and activity99

Protects muscles from atrophy by targeting atrogin-1/MAFbx1 and MURF-1. Overexpression counteracts muscle atrophy induced by dexamethasone in myotubes and glucocorticoids in mice100

VAT, SAT96

Vastus lateralis70, 98, 99

Mice99, 100

Adipocytes96

C2C12 cells100

Atrogin-1/MAFbx1100

MURF-1100

PGC-1α99, 101

Vastus lateralis MiR-424-5p (miR-322) MiR-424, miR-503, miR-542, miR-450a-2, miR-450a-1, miR-450b ↑

Down-regulated in young women with PCOS (n = 24).43 No difference between obese (n = 21) and NW (n = 19) women but correlated with waist circumference102

Increased in cachectic cancer patients103

Up-regulated in muscle wasting conditions—ICU-acquired weakness and COPD. Overexpression causes a reduction in muscle diameter of mice33

Saturated fat/high-fat diet impairs insulin signalling (INSR and IRS-1) and up-regulated miR-424-5p in hepatocytes and mice. Overexpression causes a significant decrease in insulin-induced glycogen synthesis in hepatocytes. INSR is a direct target104

Targets IGF-1 in mice and human myocytes105

Serum43

Mice33, 104

Vastus lateralis33, 103

SAT102

Plasma102

Hepatocytes104

C2C12 cells105

Human myoblasts105

SMAD733

INSR104