Hormonal
Hyperinsulinemia acts as an upstream driver of the transition from MHO to MUO by promoting excessive fat accumulation and insulin resistance, and therapies that suppress insulin secretion (e.g., diazoxide, octreotide) may prevent this progression.
If you have MHO and high insulin levels, consider strategies to reduce insulin secretion. This may involve dietary changes (e.g., low carbohydrate, intermittent fasting) or, in some cases, medications that suppress insulin (like diazoxide or octreotide, though these are not standard first-line treatments). Discuss with your doctor whether your insulin levels are driving your metabolic risk.
Increasing evidence from pre-clinical and clinical studies support a view, at least in subsets of at-risk individuals, that hyper-responsiveness of the islet β-cell to a hostile environment (e.g., from a westernised lifestyle) drives hyperinsulinemia, and the hyperinsulinemia is upstream to excessive weight gain and MetS, including the development of IR. ... Pharmacological approaches with diazoxide or the somatostatin analogue octreotide-LAR to suppress insulin secretion in humans, also support the view that hyperinsulinemia may have more of a primary role in MetS.
Why this rating
Supported by pre-clinical models and human studies using insulin-suppressing drugs, though large-scale long-term trials are not detailed in this review.
Source
Exploring Therapeutic Targets to Reverse or Prevent the Transition from Metabolically Healthy to Unhealthy Obesity
Tenzin Dagpo et al. · Cells · 2020
DOI 10.3390/cells9071596
More from this paper
- Prevention and reversal of the transition from metabolically healthy obesity (MHO) to metabolically unhealthy obesity (MUO) requires multifaceted interventions targeting both adipose tissue intrinsic factors (e.g., promoting adipogenesis) and extrinsic drivers (e.g., hyperinsulinemia, circadian disruption), with lifestyle changes serving as the foundation but often requiring pharmacological or surgical augmentation for substantial weight loss and metabolic correction.Good
- Promoting adipogenesis (the creation of new, functional adipocytes) through therapeutic agents can improve lipid storage capacity and prevent the transition from MHO to MUO by avoiding adipocyte dysfunction, hypoxia, and inflammation.Moderate
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