This concept captures the mutual regulation between HSL and insulin described throughout the review. It is useful as a curation label for literature on lipolysis-insulin crosstalk in metabolic disease.
First-pass extracted concept
HSL-insulin regulatory axis
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Evidence Snippets
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Linked Claims
Insulin's inhibitory effect on HSL can be overridden in the context of insulin-induced hypoglycemia.
a rapid elevation of HSL levels was detected after insulin injection in patients, which suggests that the inhibitory effects of insulin on HSL can be overridden by insulin-induced hypoglycemia
Hereditary HSL deficiency and experimental HSL deletion are associated with disrupted insulin signaling and metabolic disease phenotypes including insulin resistance, diabetes, and fatty liver.
individuals with hereditary HSL deficiency, and animals with experimental HSL deletion, showed major disruptions in mRNA/protein expression in insulin signaling pathways, ultimately leading to insulin resistance, diabetes, and fatty liver
HSL inactivation can cause insulin-independent fatty liver, and HSL-deficiency-associated insulin resistance may further worsen disease progression.
HSL inactivation could cause insulin-independent fatty liver, while insulin resistance induced by HSL deficiency may further aggravate disease progression.
Recent discoveries challenge the assumptions that HSL is the overall rate-limiting enzyme in lipolysis and that insulin is simply an inhibitor of HSL.
The common beliefs that HSL is the overall rate-limiting enzyme in lipolysis and that insulin is an inhibitor of HSL have been challenged by recent discoveries
Insulin regulates HSL at multiple levels including isoform transcription, post-transcriptional phosphorylation effects involving PKA and endothelin, and indirect control through growth hormone activity.
Insulin not only differentially regulates HSL isoform transcription but also post-transcriptionally affects HSL phosphorylation by stimulating PKA and endothelin (ET-1), and controls its expression indirectly via regulating the activity of growth hormone (GH).
Insulin tightly regulates hormone-sensitive lipase through central and peripheral mechanisms.
HSL is tightly controlled by insulin regulation via the central and peripheral systems.