This review presented ethnic characteristics of type 2
diabetes in Pacific Island adults in New Zealand. Diabetes mellitus is one out
of four non-communicable diseases (NCDs), which represents a set of metabolic
disorders with chronic hyperglycaemia due to defects of insulin secretion,
insulin action, or both. If left untreated or undiagnosed, diabetes mellitus
leads to confusion, coma, or death due to ketoacidosis. Pacific Island people
in New Zealand with a specific Polynesian phenotype originate from the islands
in the Pacific Ocean such as Samoa, the Cook Islands, Tonga, Niue, Tokelau,
Papua New Guinea, Vanuatu, Kiribati, Fiji, Solomon Islands, Nauru, and French
Polynesia. Therefore, they may have similar genetic and cultural origins.
Pacific Island populations were attracted to New Zealand by the prospect of
employment and were welcomed as a solution to workforce shortages in unskilled
and semi-skilled occupations. About 42% of the Pacific population live in the
10% most deprived areas of the country, with poorer housing and overcrowding,
which suggests that the incidence of diabetes is higher for people living in
the most deprived areas, compared with people living in the least deprived
areas. Socioeconomic inequalities, low education and unemployment create
remarkable psychological distress. Changes in diet rich in sugars, tobacco use,
and harmful use of alcohol have resulted in a profound reduction in physical
activity and increased obesity rates in adults and children. The “thrifty
genotype” hypothesis can explain the current increase in the prevalence of
obesity in New Zealanders of Polynesian descent.
Obesity and type 2 diabetes are major challenges for Pacific
Island adults, and they still have comparatively higher rates of obesity (68%)
and diagnosed diabetes (13%), ten years earlier than any other ethnic group in
New Zealand. Overweight and obesity have been linked to lower serum 25-OHD
concentrations, impaired insulin action, glucose metabolism, and various
metabolic processes in adipose and lean (muscle) tissue. Central or visceral
fat is more metabolically active than subcutaneous fat, causing dysmetabolism
of fatty acids and increased influx of free fatty acids into the splanchnic
circulation. Besides storing fat, adipose tissue releases molecules commonly
referred to as adipokines which may support β- cell failure and the development
of type 2 diabetes in Pacific people. Antihypertensive and anti-lipid (statin)
therapy was lowest among Pacifica people. The blood levels of triglycerides
were the lowest in the Pacific population. However, HbA1C was significantly
higher among Pacific people than among Māori, who had higher HbA1C than New
Zealand Europeans. Interestingly, as a group, Pacific Island populations are
neither hyperinsulinaemic nor insulin-resistant using HOMA-IR. This Polynesian
phenotype is linked to the metabolic disorders of gout and type 2 diabetes
mellitus, due to the presence of visceral obesity owing to its strong
association with insulin resistance, metabolic syndrome, type 2 diabetes, and
cardiovascular disease.
Author(s)details:-
Dr. Ljiljana M.
Jowitt
Faculty of Health and Environmental Sciences, School of Public Health and
Interdisciplinary Health Studies, Auckland University of Technology, New
Zealand.
Please See the book
here :- https://doi.org/10.9734/bpi/rudhr/v8/704
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