The core component of IGF 1 LR3 Tablet, IGF-1 LR3 (Long R3-IGF-1), is an artificially synthesized insulin-like growth factor-1 analog commonly used in scientific research or specific medical settings in the form of injections.
It activates downstream signaling pathways (such as AKT and MAPK) by binding to tyrosine kinase type receptors (IGF-1R), promoting cell proliferation, differentiation, and metabolic regulation. As a growth additive, IGF-1 LR3 significantly increases the proliferation rate and recombinant protein production of HEK293, CHO and other cells, and is widely used in the biopharmaceutical industry. In transgenic mouse models, LR3 is used to study muscle development, metabolic regulation, and aging mechanisms. For example, long-term injection of LR3 can delay muscle atrophy and improve the motor ability of elderly mice.
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IGF 1 LR3 COA
The insulin-like growth factor-1 long-acting analog (IGF 1 LR3 Tablet) has become a core tool peptide for the study of fat metabolism and obesity mechanisms due to its core pharmacokinetic advantages of half-life of 20-30 hours, almost no binding to IGFBPs, and free activity>95%.
The core molecular mechanism of IGF-1 LR3 regulating fat metabolism
IGF-1 LR3 regulates fat metabolism from five dimensions: lipolysis, adipogenesis, adipocyte differentiation, insulin sensitivity, and white adipose browning, by activating IGF1R → activating the PI3K/Akt and MAPK/ERK dual pathways, forming a complete regulatory network of "inhibiting synthesis, promoting decomposition, regulating differentiation, increasing sensitivity, and promoting thermogenesis".
Directly promote fat breakdown
Activate key lipolytic enzymes
After binding to adipocyte IGF1R, IGF-1 LR3 activates the PI3K/Akt pathway, phosphorylating hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGL):
ATGL: catalyzing the hydrolysis of triglycerides (TG) to diglycerides (DG), rate limiting step;
HSL: catalyzing the hydrolysis of DG into free fatty acids (FFA) and glycerol, the core step;
Activation of Akt inhibits phosphorylation of FoxO1, downregulates lipoprotein lipase (LPL) and adipocyte fatty acid binding protein (FABP4):
LPL: Inhibits FFA uptake and fat storage in the blood;
FABP4: Reduce FFA transport and deposition in adipocytes;
Effect: Fat storage is reduced by 40% -60%, forming a bidirectional regulation of "promoting decomposition and inhibiting storage".
Inhibit fat production (reduce the formation of new fat cells)
Downregulate key transcription factors involved in fat synthesis
Activation of MAPK/ERK pathway, inhibition of peroxisome proliferator activated receptor gamma (PPAR gamma) and CCAAT/enhancer binding protein alpha (C/EBP alpha)
Effect: The differentiation rate of preadipocytes decreases by 40% -70%, and the number of new adipocytes decreases.
Inhibition of fat synthase
Akt pathway downregulates fatty acid synthase (FAS) and stearoyl CoA desaturase 1 (SCD1):
FAS: catalyzing the synthesis of fatty acids from acetyl CoA;
SCD1: catalyzes the conversion of saturated fatty acids into unsaturated fatty acids;
Effect: Fatty acid synthesis in adipocytes is reduced by 50% -80%, and TG synthesis is inhibited.
Improving insulin sensitivity
Promote glucose transport to muscles
IGF 1 LR3 Tablet preferentially activates muscle IGF1R, promotes GLUT4 translocation, increases muscle glucose uptake by 2-3 times, and reduces glucose diversion to adipose tissue.
Reduce insulin levels
Increased muscle glucose uptake → decreased blood sugar → decreased insulin secretion → relief of hyperinsulinemia:
Insulin is a potent fat synthesis hormone, with a 30% -50% decrease in insulin levels leading to significant inhibition of fat synthesis;
Effect: Obesity model reduces insulin resistance index (HOMA-IR) by 40% -60%.
Reduce inflammation of adipose tissue
Inhibit the release of inflammatory factors such as TNF - α and IL-6 in adipocytes, improve insulin signaling in adipose tissue, and break the vicious cycle of "obesity → inflammation → insulin resistance → fat accumulation".
Regulating adipocyte differentiation (reducing the number of adipocytes)
Inhibition of preadipocyte proliferation: moderate activation of MAPK/ERK pathway inhibits excessive preadipocyte proliferation;
Blocking differentiation and maturation: Downregulating PPAR γ/C/EBP α to prevent preadipocytes from differentiating into mature adipocytes;
Promote adipocyte apoptosis: High dose IGF-1 LR3 (≥ 100nM) activates caspase-3/9, inducing apoptosis of mature adipocytes;
Effect: The total number of adipocytes decreases by 30% -50%, reducing fat accumulation from both the "quantity+volume" dimensions.
Promote browning of white fat (increase energy consumption)
Upregulation of brown fat markers
Activate the PI3K/Akt pathway, upregulate UCP1, PGC-1 α, and PRDM16 in white adipocytes
PGC-1 α/PRDM16: white adipose browning core transcription factor;
Effect: The expression of UCP1 in white adipose tissue is increased by 2-4 times, and heat production is increased by 30% -50%.
Activate brown adipocytes
Directly activate IGF1R in brown adipocytes, promote brown adipocyte proliferation and activation, increase systemic energy expenditure, and reduce body fat percentage.
Research applications in in vitro adipocyte models
IGF 1 LR3 Tablet is a standard tool reagent for 3T3-L1 preadipocytes, human preadipocytes, and mature white/brown adipocyte models, used to analyze fat metabolism mechanisms, screen fat loss targets, and validate drug action pathways.
3T3-L1 preadipocyte model
Research on Inhibiting Differentiation and Fat Production
Experimental protocol: 3T3-L1 cell inoculation → differentiation induction (MDI medium) → addition of IGF-1 LR3 (10-100nM) → detection on the 8th day of differentiation;
Core indicators:
Oil red O staining: lipid droplet area decreases by 40% -70%, and differentiation rate decreases;
Research on promoting lipolysis of mature adipocytes
Experimental protocol: 3T3-L1 differentiation and maturation (day 8) → serum starvation for 24 hours → addition of IGF-1 LR3 (20-100nM) → 24-hour detection;
Core indicators:
Glycerol release: increased by 50% -80% (lipolysis rate);
FFA release: increased by 40% -70%;
Protein phosphorylation: HSL (Ser660) and Akt (Ser473) phosphorylation increase by 2-3 times;
Purpose: To analyze the lipolysis signaling pathway, verify the function of HSL/ATGL, and screen drugs that promote lipolysis.
Research on Browning of White Fat
Experimental protocol: 3T3-L1 mature adipocytes → addition of IGF-1 LR3 (50nM)+differentiation medium → detection on day 6;
Core indicators:
Gene expression: UCP1, PGC-1 α, PRDM16 mRNA increase by 2-4 times;
Protein expression: UCP1 protein increases by 1-3 times;
Mitochondrial function: mitochondrial membrane potential increases, oxygen depletion rate (OCR) increases by 30% -50%;
Purpose: To study the browning mechanism of white adipose tissue, develop thermogenic fat loss strategies, and validate the UCP1 regulatory pathway.
Human derived adipocyte model
Subcutaneous/visceral preadipocytes in humans
Effect: Inhibit differentiation (reduce lipid droplets by 50%), promote lipolysis (increase glycerol release by 60%), upregulate UCP1 (2.5-fold);
Difference: visceral adipocytes are more sensitive to IGF-1 LR3 (with a 70% increase in lipolysis rate compared to subcutaneous 50%);
Purpose: To simulate human obesity fat metabolism, verify racial differences, and screen humanized fat reducing drugs.
Fat cells in obese patients
Effect: Improve insulin resistance (increase glucose uptake by 40%), reduce inflammatory factors (decrease TNF - α by 50%), promote lipolysis;
Purpose: To investigate the mechanism of abnormal fat metabolism in obese patients and evaluate the intervention effect of IGF-1 LR3 on pathological adipocytes.
Brown adipocyte model
Model: Mouse primary brown adipocytes, human brown adipocytes;
Effect: Promotes proliferation (30% increase in cell count), activation (3-fold increase in UCP1), and thermogenesis (50% increase in OCR);
Purpose: To study the activation mechanism of brown adipose tissue, develop thermogenic and fat reducing drugs, and analyze the energy metabolism regulatory network.
Advantages of in vitro model application
Long term stability: 24-hour continuous effect, no need for frequent administration, suitable for long-term differentiation experiments;
High activity: It can take effect at 10nM and has no cytotoxicity at low concentrations;
Low interference: Almost does not bind to serum IGFBPs, with good reproducibility and small errors in experimental results.
Scientific applications in animal models of obesity in vivo
IGF-1 LR3 is a core intervention reagent for high-fat diet (HFD) obese mice, db/db diabetes obese mice, ob/ob leptin deficient obese mice, and foodborne obese rat models, which is used to verify the mechanism of fat reduction, evaluate the effect of body fat regulation, and study the association of metabolic diseases.
Animal: C57BL/6 mice, 6 weeks old, fed a high-fat diet (60% fat) for 8 weeks to establish an obesity model;
Grouping: Control group (physiological saline), low-dose IGF-1 LR3 (20 μ g/kg/day), medium dose (50 μ g/kg/day), high-dose (100 μ g/kg/day);
Administration: Subcutaneous injection, once a day, lasting 4-8 weeks;
Detection indicators: body weight, body fat percentage, visceral fat weight, blood glucose, insulin, blood lipids, and gene/protein expression in adipose tissue.
Core weight loss effect (4-week intervention)
Weight loss: 8% -15% (medium dose 12%);
Body fat percentage: reduced by 15% -25% (medium dose 20%);
Visceral fat: reduced by 25% -35% (epididymal fat, perirenal fat);
Subcutaneous fat: reduce by 10% -20%;
Blood lipids: TG decreased by 30% -40%, cholesterol decreased by 20% -30%, FFA decreased by 40% -50%.
Mechanism validation (adipose tissue testing)
Lipolysis pathway: phosphorylation of HSL/ATGL increases by 2-3 times;
Db/db diabetes obese mouse model
Model features: leptin receptor deficiency, severe obesity, hyperglycemia, insulin resistance, fatty liver;
Intervention effect (6 weeks):
Weight: Decrease by 10% -18%;
Body fat percentage: reduced by 20% -30%;
Blood sugar: Fasting blood sugar decreases by 30% -40%;
Insulin: Insulin levels decrease by 40% -50%;
Fatty liver: reduces liver fat content by 30% -50%, improves liver steatosis;
Purpose: To investigate the mechanism of obesity combined with insulin resistance/fatty liver and evaluate the intervention effect of IGF-1 LR3 on metabolic syndrome.
Ob/ob leptin deficient obese mouse model
Model features: leptin gene deficiency, spontaneous obesity, hyperinsulinemia, and excessive fat accumulation;
Intervention effect (4 weeks):
Visceral fat: reduced by 30% -40%;
Fat cell size: reduced by 20% -30%;
Inflammatory factors: TNF - α/IL-6 in adipose tissue decreased by 40% -60%;
Purpose: To analyze the cross regulation of leptin and IGF-1 pathways and study the abnormal fat metabolism in congenital obesity.
Foodborne obesity rat model
Model: SD rats fed a high-fat diet for 12 weeks;
Intervention effect (8 weeks):
Weight: Decrease by 10% -15%;
Body fat percentage: reduced by 18% -25%;
Insulin sensitivity: increased by 30% -40%;
Advantages: Rat fat metabolism is closer to that of humans, with sufficient sample size, suitable for long-term intervention experiments.
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