Lyrics · 完整歌詞
Glucose homeostasis depends on the coordinated, opposing actions of insulin and glucagon,
both secreted within the pancreatic islets.
Beta cells release insulin,
which drives glucose into muscle and fat and suppresses hepatic gluconeogenesis.
Alpha cells release glucagon, which mobilises hepatic glycogen and raises glucose.
Glucagon can therefore be used to treat severe hypoglycaemia;
its glucose-raising action does not make it a treatment for hyperglycaemia.
Diabetes is diagnosed when fasting glucose is at least 7.0 mmol/L,
a two-hour or random value reaches 11.1 mmol/L,
or HbA1c reaches 6.5 per cent.
Type 1 disease is autoimmune insulitis with absolute insulin deficiency
and antibodies to GAD65 and IA-2.
Type 2 disease is insulin resistance with relative deficiency,
and islet amyloid derived from amylin fills the islets of most patients.
Insulin resistance rarely travels alone.
The metabolic syndrome is diagnosed when three of five features coexist:
central obesity, raised triglycerides, low HDL cholesterol,
raised blood pressure and impaired fasting glucose.
LDL cholesterol is deliberately absent from the list.
Insulin resistance changes the quality of lipoproteins, producing small dense LDL particles,
rather than raising the LDL concentration.
Consequently, a waist of 108 centimetres,
triglycerides of 2.4 mmol/L
and HDL of 0.9 mmol/L announce the syndrome before glucose rises far.
Glucose homeostasis depends on the coordinated, opposing actions of insulin and glucagon,
both secreted within the pancreatic islets.
Metformin remains first line
because it suppresses hepatic glucose output without provoking hypoglycaemia.
Its hazards are lactic acidosis in renal failure,
so it is withheld around iodinated contrast
and avoided below an eGFR of 30,
and vitamin B12 deficiency after years of use.
The choice of the second agent is now decided by the organs
at risk rather than by HbA1c alone.
SGLT2 inhibitors and GLP-1 receptor agonists reduce weight and protect the kidney
and heart,
whereas DPP-4 inhibitors are weight neutral.
Sulfonylureas carry the highest hypoglycaemia risk, pioglitazone is contraindicated in heart failure,
and thiazide diuretics raise glucose without ever causing hypoglycaemia.
The earliest sign of diabetic kidney disease is microalbuminuria,
detected as an albumin-to-creatinine ratio above 2.5 mg/mmol in men
and 3.5 mg/mmol in women.
At this stage creatinine and eGFR are still normal,
and an ACE inhibitor or angiotensin receptor blocker slows progression.
Retinopathy is screened by retinal photography, neuropathy by the ten-gram monofilament,
and vessels are protected by blood pressure below 130/80 mmHg
and LDL below 1.8 mmol/L.
When a diabetic foot ulcer overlies bone,
bone biopsy rather than a surface swab remains the gold standard for osteomyelitis.
Targets must fit the person.
A general adult aims for an HbA1c below 7.0 per cent,
and a young patient with short disease duration may aim below 6.5.
A frail octogenarian is safer at 8.0 to 8.5 per cent,
because hypoglycaemia causes falls, arrhythmias and cognitive harm.
Hypoglycaemia itself is most often caused by sulfonylureas or insulin,
not by insulinoma.
The conscious patient takes fifteen grams of glucose
and rechecks in fifteen minutes;
the unconscious patient receives intravenous dextrose or intramuscular glucagon.
C-peptide separates the causes:
it is high with insulinoma and low when insulin has been injected.
Glucose homeostasis depends on the coordinated, opposing actions of insulin and glucagon,
both secreted within the pancreatic islets.