The association of PTEN/PI3K/Akt pathway gene expression with insulin indices in adipose tissues of non-diabetic female adults: a cross-sectional study
Bibliographic record
Abstract
Insulin resistance (IR) is a complex metabolic condition that serves as a common thread connecting type 2 diabetes (T2DM), metabolic syndrome (MetS), cardiovascular disease (CVD), and even certain cancer outcomes. Understanding and addressing IR is crucial for the prevention and management of these interrelated health challenges. Adipose tissue (AT) is one of the main targets for insulin action, and insulin suppresses lipolysis in this tissue. This study aimed to investigate the relationship between genes in the PI3K/AKT pathway and the negative regulator of this pathway, PTEN, with indices of insulin resistance in human adipose tissue. In this cross-sectional study, 118 women, aged ≥ 18 years were selected among patients who were admitted to hospitals (Mostafa Khomeini and Khatam Al-Anbia, Tehran, Iran) for elective and minimal abdominal surgery including appendectomy and umbilical and inguinal hernia repair. Anthropometric and laboratory parameters, physical activity, and dietary intake were measured. Expression of PTEN, PI3K, and Akt genes were evaluated using Real-Time qRT-PCR. Insulin-related metabolic indices such as hyperinsulinemia, HOMA-IR, HOMA-B, HOMA-S, QUICKI, and TyG indexes were defined and calculated. After controlling age, physical activity, BMI, and energy intake, the expression of SAT PTEN was negatively associated with IR (β=-4.475, P = 0.021) and positively associated with HOMA-B cell dysfunction (β = 4.944, P = 0.012). VAT PI3K was positively associated with hyperinsulinemia (β = 8.802, P = 0.008) and IR (β = 7.710, P = 0.028). Higher VAT Akt gene expression was associated with higher hyperinsulinemia (β = 6.684, P = 0.003) and IR (β = 5.296, P = 0.027). Moreover, higher SAT Akt mRNA level was associated with FPI (β = 0.128, P = 0.048), and hyperinsulinemia (β = 4.201, P = 0.008). The findings of the present study suggest that hyperinsulinemia and insulin resistance (HOMA-IR), are directly associated with PI3K and Akt expression yet they show an inverse relationship with PTEN, which inhibits the insulin pathway.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.001 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".