Step 1: In type 1 diabetes the pancreatic beta cells fail and circulating insulin is essentially absent, so insulin-dependent metabolic controls are switched off.
Step 2: Without insulin, hormone-sensitive lipase in adipose tissue stays active. This means triglyceride stores are continuously hydrolysed, a process called lipolysis, releasing free fatty acids into the blood.
Step 3: These fatty acids flood the liver and undergo heavy beta-oxidation. Acetyl-CoA produced beyond the capacity of the TCA cycle is diverted to ketone body synthesis, explaining the ketosis seen in uncontrolled disease.
Step 4: Reviewing the distractors: tissue glucose uptake falls because GLUT4 needs insulin, hepatic glucose release rises from unchecked gluconeogenesis and glycogenolysis, and muscle protein catabolism increases to supply gluconeogenic substrates. The only correct statement is the rise in lipolysis.\[\boxed{\text{Increased lipolysis}}\]