Health Claims

When diabetic rats are given insulin, their kidneys excrete less uric acid, and the levels of key uric acid transporters (URAT1 and ABCG2) return to normal, which helps explain why insulin can affect uric acid levels. This finding is from the abstract summary - full study details were not available

In diabetic rats, the kidneys show lower levels of the URAT1 transporter and higher levels of the ABCG2 transporter in the membrane parts of kidney cells, which helps explain why more uric acid is excreted. This finding is from the abstract summary - full study details were not available

When rats have diabetes caused by streptozotocin, their kidneys excrete more uric acid than normal rats, which means their bodies are getting rid of more uric acid through urine. This finding is from the abstract summary - full study details were not available

Higher uric acid levels were linked to lower availability of nitric oxide, a molecule important for blood vessel function. This finding is from the abstract summary - full study details were not available

Eating fructose (like table sugar) led to higher uric acid levels in rats compared to other sugars. This finding is from the abstract summary - full study details were not available

Higher levels of uric acid made blood vessels less able to widen in response to a chemical signal, which could affect blood flow. This finding is from the abstract summary - full study details were not available

In rats eating a high-fructose diet, drugs that lower uric acid (allopurinol or benzbromarone) were linked to lower levels of insulin, blood pressure, triglycerides, and weight compared to rats not receiving these drugs. This finding is from the abstract summary - full study details were not available

In rats, eating a lot of fructose (like table sugar) led to higher levels of insulin, triglycerides, and uric acid compared to eating dextrose (a different sugar), suggesting fructose might have unique effects on metabolism. This finding is from the abstract summary - full study details were not available

In mice with insulin resistance, insulin treatment caused a small, temporary rise in systolic blood pressure (about 5 mm Hg) in the first week, but blood pressure returned to normal levels after that.

In mice with insulin resistance, insulin treatment made the blood slightly more acidic, as shown by a drop in pH from 7.24 to 7.11.

In mice with insulin resistance, insulin treatment lowered blood urea nitrogen levels by about two-thirds, which may indicate changes in kidney function or diet.

In mice with insulin resistance, insulin treatment caused a significant rise in the anion gap (a measure of acid in the blood), suggesting the blood became more acidic.

In mice with insulin resistance, long-term insulin treatment raised blood sodium levels by about 5 units.

In mice with insulin resistance, giving extra insulin for two weeks lowered the levels of nitric oxide breakdown products in blood and urine by almost half, even though the kidney showed signs of producing more nitric oxide.

Leptin doesn't change how well mice with missing leptin receptors in certain brain cells regulate their blood pressure through reflexes.

Giving leptin to mice raises their leptin hormone levels to about 80 ng/ml, regardless of whether they have leptin receptors in certain brain cells.

Mice missing leptin receptors in certain brain cells have blood pressure like mice with floxed leptin receptors but lower than normal mice.

Mice missing leptin receptors in certain brain cells have twice as much belly fat as normal mice.

Leptin reduces eating in both normal mice and those missing leptin receptors in certain brain cells, meaning these brain cells aren't needed for leptin's appetite control.

Mice missing leptin receptors in certain brain cells have weaker blood pressure and heart rate reactions to sudden stress compared to normal mice.

Leptin makes both normal mice and those missing leptin receptors in certain brain cells burn more oxygen, meaning this effect works through other brain pathways.

Leptin lowers blood sugar and insulin in normal mice, but not in mice missing leptin receptors in certain brain cells.

When mice lack leptin receptors in certain brain cells, giving them leptin slightly lowers their blood pressure instead of raising it like in normal mice.

When mice lack leptin receptors in certain brain cells, they become heavier, have higher blood sugar, more insulin, and more leptin hormone than normal mice.