It may be a normal variant in the Inuit populations, just as slightly low normal white cell count is common in Mediterranean peoples, and slightly high white cell count is normal in Mexican Hispanics. But I’ll try to give some possible explanations, while confessing that these are speculative.
Thrombocytosis may be reactive — secondary to chronic inflammation/infection, iron deficiency or underlying neoplastic process; or non-reactive — also called primary thrombocytosis — in which case the platelet count is often over 600,000. Low grade thrombocytosis is often reactive, and iron deficiency is frequently an easily treatable cause that should be excluded first.
Gamma-GT (GGT) is an enzyme present in hepatocytes and biliary epithelial cells and is a very sensitive marker of hepatobiliary disease. Like most sensitive tests, its use is limited by its low specificity, as this marker can be elevated in pancreatic disease, COPD, diabetes, chronic kidney disease, obesity and alcoholism. Pharmacologic agents like phenytoin and barbiturates that induce the hepatic microsomal system can cause high GGT levels as well.
Obesity is felt to be a chronic low-grade inflammatory state, contributing to many ill-health consequences. Obesity is common in aboriginal populations. Fatty liver with mild elevation in GGT is common in obese people, and obesity-related low-grade inflammation can contribute to mild thrombocytosis in otherwise healthy individuals, as you have noted. On the other hand, progressive familial intrahepatic cholestasis (PFIC), an autosomal recessive disorder, is caused by defects in biliary epithelial transporters that often occur in childhood. The result is progressive cholestasis, failure to thrive, hepatic failure and need for liver transplantation. This is common in Inuit populations and is also known as Greenland Eskimos familial cholestasis. It’s uncertain whether carriers of PFIC mutations who are otherwise healthy have mild elevation of GGT, but it’s certainly a possibility to consider.