Recently, the international academic journal Nature Communications published a research paper online: Researchers from the University of Utah have discovered a new toxin in the venom of the deadly cone snail (Conus geographus). Its unique and sustained effects may help scientists design better drugs for treating diabetes or hormonal disorders.

This toxin has been named "consomatin."

It may seem counterintuitive to seek better drugs from a lethal venom.

Nevertheless, "the lethality of toxins often works by precisely targeting specific molecules. The same precision could prove very useful in treating diseases," said Dr. Helena Safavi, an associate professor at the Spencer Fox Eccles School of Medicine at the University of Utah and the corresponding author of the paper.

The title of the paper is “Fish-hunting cone snail disrupts prey’s glucose homeostasis with weaponized mimetics of somatostatin and insulin.”

Compared to existing somatostatin drugs for humans, consomatin displays greater specificity, which is expected to avoid unnecessary off-target effects associated with similar drugs.

Additionally, consomatin contains an unusual amino acid that makes it difficult to decompose, allowing it to persist longer and continually exert its pharmacological effects.

The geographic cone snail (Conus geographus) is a marine carnivorous mollusk, also known as the "killer cone snail." It belongs to the fish-hunting cone snails and is one of the most toxic species in the cone snail family, with venom capable of causing human death.

Venomous animals have evolved various molecular mechanisms to capture prey or defend against predators. Most venom components disrupt other organisms' nervous, muscular, and cardiovascular systems or cause tissue damage. Certain fish-hunting cone snails utilize "weaponized" insulin to induce hypoglycemic shock in their prey, highlighting the importance of glucose homeostasis.

In this latest research, scientists found that, in addition to insulin, the deadly fish-hunting conus snail employs a somatostatin receptor 2 (SSTR2) agonist—consomatin—to block the release of glucagon, thereby exacerbating the insulin-induced hypoglycemic symptoms in their prey.

Dr. Ho Yan Yeung, the first author of the paper, explained that researchers discovered that consomatin toxin specifically targets proteins that regulate glucagon levels without affecting other molecular levels.

In previous studies, the team identified another insulin-like toxin in conus snail venom, which can quickly lower the blood sugar levels of its prey.

Thus, researchers hypothesized that consomatin acts in conjunction with the aforementioned insulin-like toxin to lower the prey's blood sugar and sustain it at dangerously low levels for capturing purposes.

Dr. Yeung stated that by studying the structure of consomatin, researchers could design drugs for regulating endocrine disorders with fewer side effects.