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The results illustrated that Gln restriction led to a pronounced decline in intracellular GSH levels (Fig

eubiosis), intestinal barrier integrity, systemic inflammation, insulin resistance, dyslipidemia, adipose tissue accumulation, and immune cell responses (TLR4, TLR2, Treg, Th1, Th2, Th17), culminating in adverse obesity rather than a healthy metabolic condition

Preserving CI function with NDI1 expression maintained adipogenic and lipogenic transcription in adipocytes lacking the circadian clock

In addition to its glycolytic role, HK2 associates with mitochondrial proteins, sustaining their function and influencing apoptosis